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Biomedical subjects

M Xu

Publications and source records attributed to M Xu.

At least 235 records · Page 13Linked to original sources
PubMed1998

[Evaluation of the growth and contraction of composite skin].

OBJECTIVE: To evaluate the growth and contraction of different composite skin grafts. METHODS: The status of the following composite skin grafts was evaluated over 2 years: allogeneic sucking pig dermis and autologous epidermis (group 1, n = 19), allogeneic young pig dermis and autologous epidermis (group 2, n = 7), autologous epidermis (group 3, n = 8). The effects of gestation on the composite skin grafts were also assessed. RESULTS: It showed that composite skin grafts had smooth surface and no scar formation during 2 to 124 weeks after transplantation. After week 36, the surface area of each group enlarged with different growth rates: group 1 > group 2 > group 3 (P < 0.01). Whole piece grafting was significantly better than joining together of smaller pieces after week 24 (P < 0.001). During pregnancy, CS had good growth ability and elasticity (P < 0.01). Histological study showed that group 1 had rapid growth of skin papillae and epidermal ridges similar to normal skin at week 24. CONCLUSION: As CS graft with trypsin treated allogeneic sucking pig dermis as a substitute for dermis showed the advantages of rapid growth, good elasticity and stability, it is suggested that it could be used in clinical practice.

Animals↗
PubMed1998

[Application of capillary electrophoresis in speciation analysis].

Each species has different chemical and biological behaviors. Toxicity is often dependent on it. So element speciation is important in a variety of environmental, biological, geological, and medical applications. Recently, capillary electrophoresis(CE) has been applied to speciation analysis owing to its high efficiency and short analysis time. This paper reviews the applications of CE-UV and CE-ICP-MS in speciation analysis and discusses some related problems.

Arsenic↗
PubMed1998

[Chemical constituents of Bufo Siccus].

OBJECTIVE: To study the chemical constituents of Bufo Siccus. METHOD: Based on silica column chromatography six compounds were obtained from the alcoholic extract of Bufo Siccus and identified by physico-chemical and spectroscopic analyses. RESULT: The compounds were identified as cholesterol, beta-sitosterol, resibufogenin, cinobufagin, bufalin and gamabufotalin. CONCLUSION: Studies on the chemical constituents of Bufo Siccus were reported for the first time.

Animals↗
PubMed1998

Ultrastructural observation on spermatocytogenesis in Taeniid cestodes.

AIM: To study the spermatocytogenesis of taeniid cestodes at the ultrastructural leaves. METHODS: Transmission electron microscopy. RESULTS: The ultrastructural observation on spermatocytogenesis in Taenia solium, T. saginata and T. pisiformis were made by TEM. Two types of spermatogonia; type A and B, as well as the supporting cells surrounding the peripheral of spermatogonia are recognized. The type A spermatogonia are stem cells and the type B are mother cells which produce 16 primary spermatocytes by mitosis for 4 times with the cells unseparated. The primary spermatocytes are characterized by the ribosome masses in the cytoplasm. 32 secondary spermatocytes arranged in roselike were produced by reductive division of primary spermatocytes. The secondary spermatocytes become the spermatid quickly by short time development. CONCLUSION: The dividing mode of spermatogonia in Taeniid cestodes is mitosis with cells unseparated.

Animals↗
PubMed1998

Ultrastructural observation on the transformation of the spermatozoon in spermatogenesis of Taeniid cestodes.

AIM: To study the transformation of taeniid spermatozoon during spermatogenesis on the ultrastructure level. METHODS: Transmission electronmicroscopy. RESULTS: This paper was the second part of the ultrastructural observations on the spermatogenesis in Taeniid cestodes: The transformation of the spermatozoon. The 64-spermatid-plasmodium was generated from the secondary meiosis of the 32 rose-like secondary spermatocytes. The transformation of the spermatozoon was a complex process. Firstly, both the cytoplasm and nucleus of the spermatid elongated while the cytoplasm increased and connected to the cytoplasmic mass (cytophore). Secondly, the chromatins of nucleus polymerized to a thread-bundle-like structure. Finally, it detached from the cytoplasm mass and became a mature spermatozoon. The mature spermatozoon was a thread-like structure, about 16.2-18.6 microns in length and 0.35-0.45 micron in diameter. There were two structurally distinct parts: the part with the nucleus was the head and the part without the nucleus was the tail. The head measured about 5-6 microns in length, 1/3 of the total body length and contained an elongated nucleus which twined around the axoneme without mitochondria. The tail was about 11.2-16.6 microns in length. Throughout the core of the tail was an axoneme with typical "9 + 1" structure. The anterior of the tail, just behind the head, were some mitochondria, about 1.6-1.7 microns in total length which twined around the axoneme. The posterior of the tail contained only an axoneme. In cross-section of the spermatozoon, about 46 microtubules were beneath the plasma membrane. CONCLUSION: The transformation of the spermatozoon is a very complex process.

Animals↗
PubMed1998

Mutational screening of the bone morphogenetic protein 4 gene in a family with fibrodysplasia ossificans progressiva.

Bone morphogenetic proteins have been proposed as candidate genes for fibrodysplasia ossificans progressiva. Bone morphogenetic protein 4 is overexpressed in cells derived from these patients. The bone morphogenetic protein 4 genes from a family showing autosomal dominant inheritance of fibrodysplasia ossificans progressiva have been screened for mutations by single strand conformation polymorphism analysis and deoxyribonucleic acid sequencing. The exon coding regions and splice junctions of the bone morphogenetic protein 4 gene have been examined for polymorphisms in all five family members. However, no mutation was discovered in these messenger ribonucleic acid and protein coding regions or in the splice junctions of affected or unaffected family members. In addition, approximately 1.5 kb of upstream flanking sequences also were examined. Neutral polymorphisms were identified in the upstream flanking region of the bone morphogenetic protein 4 gene. Although this study has not identified any mutations in the bone morphogenetic protein 4 gene that are correlated with the occurrence of fibrodysplasia ossificans progressiva, the bone morphogenetic protein 4 gene cannot yet be excluded from consideration as the genetic cause of this disorder because a mutation could be present in unexamined regulatory sequences of this gene.

Bone Morphogenetic Protein 4↗
PubMed1998

The effects of qi-gong and acupuncture on human cerebral evoked potentials and electroencephalogram.

Although a number of studies on traditional Chinese medicine, such as qi-gong (QG), acupuncture (AC), moxibustion and Chinese herbal drugs, have been reported in recent years, there are few reports on human cerebral evoked potentials (EPs), especially relating only to QG and AC. In the present study, we examined the changes in EPs and electroencephalogram (EEG) by QG, and by AC stimulation to the point called "Zusanli" on the left lower leg, with one healthy male adult. 1. With regard to the effect of QG, significant changes in EP-components originated from the cortex suggest both facilitating and inhibitory effects of QG on the cortex. However, no significant changes in EP-components originated from the subcortex and no significant changes in EEG power% suggest that QG does not affect the subcortex. 2. With regard to the effects of AC, significant changes in EP-components originated from the cortex suggest facilitating and inhibitory effects of AC stimulation on the cortex. Furthermore, it is suggested that AC stimulation has few effects on the somatosensory and the visual pathways up to the cortex, while it has complicated effects on the auditory pathway up to the cortex.

Acupuncture Therapy↗
PubMed1997

Thiazolidinediones block tumor necrosis factor-alpha-induced inhibition of insulin signaling.

TNF-alpha has been shown to be an important mediator of insulin resistance linked to obesity. This cytokine induces insulin resistance, at least in part, through inhibition of the tyrosine kinase activity of the insulin receptor. Recently, a new class of compounds, the antidiabetic thiazolidinediones (TZDs), has been shown to improve insulin resistance in obesity and non-insulin-dependent diabetes mellitus in both rodents and man. Here we show that TZDs have powerful effects on the ability of TNF-alpha to alter the most proximal steps of insulin signaling, including tyrosine phosphorylation of the insulin receptor and its major substrate, IRS-1, and activation of PI3-kinase. Troglitazone or pioglitazone essentially eliminate the reduction in tyrosine phosphorylation of IR and IRS-1 caused by TNF-alpha in fat cells, even at relatively high doses (25 ng/ml). That this effect of TZDs operates through activation of the nuclear receptor PPARgamma/ RXR complex is shown by the fact that similar effects are observed with other PPARgamma/RXR ligands such as 15 deoxy Delta12,14PGJ2 and LG268. The TZDs do not inhibit all TNF-alpha signaling in that the transcription factor NF-kB is still induced well. These data indicate that TZDs can specifically block certain actions of TNF-alpha related to insulin resistance, suggesting that this block may contribute to their antidiabetic actions.

3T3 Cells↗
PubMed1997

Identification of the transcriptional repression domain of nuclear factor 1-A.

We previously showed that nuclear factor 1-A (NF1-A) binds to the silencer elements in the glutathione transferase P (GST-P) gene, and the carboxy terminal region of NF1-A represses the transcription activity of human metallothionein IIA (hMTIIA) promoter. In this study, we identified a repression region which is divided into two 100 amino acid domains (RD1 and RD2). RD1 increased the repression activity of RD2 to the hMTIIA promoter activity. The NF1-A repression domain inhibited the promoter activities of not only the hMTIIA gene but also those of the GST-P and CCAAT/enhancer binding protein delta genes. RD1 and RD2 had abundant serine and glycine residues, and proline and serine residues, respectively. Whereas some repression domains identified previously are enriched with alanine, proline, or serine, and are associated with the general transcription factors, the NF1-A repression domains did not interact with transcription factor IIB, TATA-binding protein (TBP), or TBP-associated factors in vitro.

CCAAT-Enhancer-Binding Proteins↗
PubMed1997

Steroid-induced conformational changes at ends of the hormone-binding domain in the rat glucocorticoid receptor are independent of agonist versus antagonist activity.

The underlying molecular mechanism for the expression of agonist versus antagonist activity for a given receptor-steroid complex is still not known. One attractive hypothesis, based on data from progesterone receptors, is that agonist versus antagonist binding induces unique conformations at the C terminus of receptors, which can be detected by the different fragments produced by partial proteolysis. We now report that the determinants of glucocorticoid receptor (GR)-antagonist complex activity are more complex. Steroid binding did cause a conformational change in the GR that was detected by partial trypsin digestion, as described previously (Simons, S. S., Jr., Sistare, F. D., and Chakraborti, P. K. (1989) J. Biol. Chem. 264, 14493-14497). However, there was no uniformity in the digestion patterns of unactivated or activated receptors bound by a series of six structurally different antagonists including the affinity labeling antiglucocorticoid dexamethasone 21-mesylate. A total of four resistant bands were observed on SDS-polyacrylamide gels in the range of 30-27 kDa. Using a series of point mutations and epitope-specific antibodies, it was determined that the 30-kDa species represented the entire C-terminal sequence of amino acids 518-795, whereas the other bands arose from additional N-terminal and/or C-terminal cleavages. Bioassays with GRs containing various point and deletion mutations failed to reveal any C-terminal alterations that could convert antagonists into biologically active agonists. Thus, the presence or absence of C-terminal amino acids of the GR did not uniquely determine either the appearance of smaller trypsin-resistant fragments or the nature of the biological response of receptor-bound antisteroids. When compared with the current model of the ligand-binding domain, which is based on the x-ray structures of the comparable region of thyroid and retinoic acid receptors, the present results suggest that sequences outside of the model structure are relevant for the binding and biological activity of GRs.

Animals↗
PubMed1997

Alzheimer presenilins in the nuclear membrane, interphase kinetochores, and centrosomes suggest a role in chromosome segregation.

Mutations in two related genes, presenilin 1 and 2, account for most early-onset familial Alzheimer's disease. Although structural features indicate that the presenilins are membrane proteins, their function(s) is unknown. We have localized the presenilins to the nuclear membrane, its associated interphase kinetochores, and the centrosomes-all subcellular structures involved in cell cycle regulation and mitosis. The colocalization of the presenilins with kinetochores on the nucleoplasmic surface of the inner nuclear membrane, together with other results, suggests that they may play a role in chromosome organization and segregation, perhaps as kinetochore binding proteins/receptors. We discuss a pathogenic pathway for familial Alzheimer's disease in which defective presenilin function causes chromosome missegregation during mitosis, resulting in apoptosis and/or trisomy 21 mosaicism.

Alzheimer Disease↗
PubMed1997

PPARgamma induces cell cycle withdrawal: inhibition of E2F/DP DNA-binding activity via down-regulation of PP2A.

PPAR gamma is an adipose-selective nuclear hormone receptor that plays a key role in the control of adipocyte differentiation. Previous studies indicated that activation of ectopically expressed PPAR gamma induces differentiation when cells have ceased growth because of confluence. We show here that ligand activation of PPAR gamma is sufficient to induce growth arrest in fibroblasts and SV40 large T-antigen transformed, adipogenic HIB1B cells. Cell cycle withdrawal is accompanied by a decrease in the DNA-binding and transcriptional activity of the E2F/DP complex, which is attributable to an increase in the phosphorylation of these proteins, especially DP-1. This effect is a consequence of decreased expression of the catalytic subunit of the serine-threonine phosphatase PP2A. These data suggest an important role for PP2A in the control of E2F/DP activity and a new mode of cell cycle control in differentiation.

3T3 Cells↗
PubMed1997

Parenteral gene therapy with p53 inhibits human breast tumors in vivo through a bystander mechanism without evidence of toxicity.

Mutations of the p53 tumor suppressor gene are the most frequently observed genetic lesion in human cancer. Previously, we found that multiple intravenous injections of a liposome:p53 complex inhibited the growth of a malignant human breast cancer cell line that was implanted into nude mice. In the present study, we evaluated the toxicity of the liposome:p53 complex and the mechanism of this in vivo treatment in reducing tumor growth. Intravenously delivered liposome:p53 complex at dosages sufficient to inhibit human breast cancer in nude mice showed no evidence of toxicity. Clinical chemistries, complete blood counts, and histopathologic examination of various organs from the p53-treated groups did not demonstrate any difference from the control groups. To elucidate the mechanism by which the liposome:p53 complex inhibits cancer, the transfection efficiency of a liposome:chloramphenicol acetyltransferase (CAT) complex into the tumor was determined. Interestingly, less than 5% of the tumor was transfected with a liposome:CAT complex. A mechanism that could account for p53 reduction of tumor size and a low transfection efficiency is inhibition of angiogenesis. After one treatment, we found that the liposome:p53 complex reduced the number of blood vessels in the p53-treated group by approximately 60% compared to the control group (p < 0.001). The close correlation between the antitumor effect of p53 and the reduction of blood vessel density in the tumor suggests that p53 effects are mediated, at least in part, by an antiangiogenesis mechanism.

Animals↗
PubMed1997

Effects of tea and chlorophyllin on the mutagenicity of N-hydroxy-IQ: studies of enzyme inhibition, molecular complex formation, and degradation/scavenging of the active metabolites.

Green tea and black tea inhibit the formation of carcinogen-DNA adducts and colonic aberrant crypts in rats given 2-amino-3-methylimidazo[4, 5-f]quinoline (IQ), a mutagen from cooked meat. The Salmonella mutagenicity assay was used in the present study to test individual constituents of tea as inhibitors of 2-hydroxyamino-3-methylimidazo[4, 5-f]quinoline (N-hydroxy-IQ), a direct-acting metabolite of IQ. Testing of pure compounds at doses relevant to their levels in tea identified epigallocatechin (EGC) and epigalocatechin-3-gallate (EGCG) as the primary antimutagens. Studies of the inhibitory mechanisms established that the rate of degradation of N-hydroxy-IQ under aqueous conditions was not increased significantly in the presence of tea, in contrast to the results obtained with the complexing agent chlorophyllin (CHL), which rapidly degraded the mutagen. Interaction between N-hydroxy-IQ and several tea constituents was detected in spectrophotometric studies, but the binding constants were only on the order of 1 x 10(3) M-1, suggesting that mechanisms other than complex formation might prevail under the conditions of the Salmonella assay. Comparison of the results in two different strains of Salmonella typhimurium, TA98 and TA98/1,8-DNP6, indicated that the antimutagenic activity of EGCG was dependent, at least in part, on a functional O-acetyltransferase activity in the bacteria. These studies suggest that tea constituents inhibit the enzyme(s) which generate the aryl nitrenium ion and directly scavenge the reactive electrophile, whereas CHL complexes with heterocyclic amines and facilitates the degradation of active metabolites.

Antimutagenic Agents↗
PubMed1997

Overexpression and large-scale production of recombinant L-methionine-alpha-deamino-gamma-mercaptomethane-lyase for novel anticancer therapy.

The goal of the next generation of cancer chemotherapy is effective tumor-selectivity. A tumor-selective target with high therapeutic potential is the elevated methionine requirement of tumor cells relative to normal cells. We have termed the elevated requirement for methionine in tumors methionine dependence. To selectively target the methionine dependence of tumors for treatment on a large-scale preclinical and clinical basis, the L-methionine alpha-deamino-gamma-mercaptomethane-lyase (methioninase, METase) gene from Pseudomonas putida has been cloned in Escherichia coli using the polymerase chain reaction (PCR). The METase gene was then ligated into the pT7-7 overexpression plasmid containing the T7 RNA polymerase promoter and recloned in E. coli strain BL21(DE3). The pAC-1 clone was isolated by its yellow-orange color which is due to high enrichment of the pyridoxal phosphate-containing recombinant methioninase (rMETase) and distinguished rMETase-overproducer from rMETase-negative colonies. A scale-up production protocol which contained a heat step, two DEAE Sepharose FF ion-exchange, and one ActiClean Etox endotoxin-affinity chromatography columns has been established. The pAC-1 clone produces rMETase at approximately 10% of the total soluble protein and up to 1 g/liter in shake-flask culture. The protocol can produce therapeutic rMETase at the multi-gram level per batch with high yield (> 60%), high purity (> 98%), high stability, and low endotoxin. Purified rMETase is stable to lyophilization. The t1/2 of rMETase was 2 h when rMETase was administered by i.v. injection in mice. Studies of the antitumor efficacy of rMETase in vitro and in vivo on human tumors xenografted in nude mice demonstrated that all types of human tumors tested including those from lung, colon, kidney, brain, prostate, and melanoma were sensitive to rMETase. In contrast, normal cells were insensitive to rMETase in vitro and correspondingly, no toxicity was detected in vivo at the effective doses. In conclusion, the overexpression clone and large-scale production protocols for rMETase have enabled rMETase to be used as a tumor-selective therapeutic with broad indication and high promise for effective, low-toxicity human cancer therapy.

Amino Acid Sequence↗
PubMed1997

Involvement of three glutamate receptor epsilon subunits in the formation of N-methyl-D-aspartate receptors mediating excitotoxicity in primary cultures of mouse cerebellar granule cells.

The N-methyl-D-aspartate receptors have been implicated in neuronal plasticity and their overactivation leads to neurotoxicity. Molecular cloning and co-expression of various glutamate receptor zeta and epsilon complementary DNAs support a heteromeric structural organization for N-methyl-D-aspartate receptors. In this study, we show that cerebellar granular neurons in primary culture of mouse express glutamate receptor zeta1 and at least three glutamate receptor epsilon (epsilon1, epsilon2, and epsilon3) protein subunits. In vitro, the temporal patterns of glutamate receptor epsilon1, epsilon2, and epsilon3 subunit expression depend on culture stages. By day 9, a somatic and neuritic immunolocalization for all N-methyl-D-aspartate subunits was clearly identified in most neuronal, but not glial cells. The role of particular subunits in N-methyl-D-aspartate-mediated excitotoxicity was probed by exposing the cerebellar granule cells to antisense oligodeoxynucleotides generated against specific N-methyl-D-aspartate receptor subunits. Antisense oligodeoxynucleotide treatments significantly down-regulated the amounts of the corresponding N-methyl-D-aspartate subunits. The decrease in N-methyl-D-aspartate subunit protein correlated with a reduction in N-methyl-D-aspartate-induced calcium influx and N-methyl-D-aspartate-mediated excitotoxicity in cerebellar cultures. In contrast, antisense oligodeoxynucleotide treatment failed to protect neurons from 1-methyl-4-phenylpyridinium-induced metabolic cell toxicity. Antisense oligodeoxynucleotide treatment targeted at N-methyl-D-aspartate glutamate receptor epsilon subunits demonstrate that glutamate receptor epsilon1, epsilon2, and epsilon3 proteins form N-methyl-D-aspartate receptors responsible for neurotoxic effects on cerebellar neurons. This study provides direct evidence for the existence of distinct N-methyl-D-aspartate receptor subunit proteins in cerebellar granule cells developing in vitro that may trigger N-methyl-D-aspartate-dependent excitotoxicity.

Animals↗