Search PubMed⌕ Search

Biomedical subjects

X W Wang

Publications and source records attributed to X W Wang.

At least 37 records · Page 2Linked to original sources
PubMed2001

Frontotemporal orbitozygomatic craniotomy to exposure the cavernous sinus and its surrounding regions. Microsurgical anatomy.

BACKGROUND: The microsurgical anatomy of the cavernous sinus and its surrounding regions were examined via frontotemporal orbitozygomatic (FTOZ) craniotomy. Combined with other deep osteotomies, the possibility of exposing the petroclival region and basilar artery was also explored. METHODS: The study was made on 20 sides of 10 cadaveric specimens fixed with formalin, with the help of the surgical microscope (magnification 5-15). RESULTS: The FTOZ was performed with frontotemporal and orbitozygomatic flaps. Extradurally, V2, V3, the trigeminal ganglion, the posterior vertical segment of the intracavernous ICA and the VI nerve were exposed by FTOZ craniotomy. By further removal of the petrous apex (Kawase's triangle), exposure could be extended to the petroclival region; with anterior modification of the microscopic light, in 50% of the specimens, exposure reached as low as the convergence of the vertebral arteries. The anterior part of the cavernous sinus and the orbital apex were examined by removing the anterior clinoid process, orbital roof and unroofing the optic canal. Intradurally, the intrapeduncular fossa (upper 1/3 of the clivus) was examined. The intracavernous cranial nerves and vessels were studied via lateral and superior wall approaches. By removing both the anterior and posterior clinoid processes together, in 80% of the specimens, the exposure could be carried as far as the midpoint of the basilar artery. CONCLUSIONS: FTOZ craniotomy could be used to treat lesions involving the cavernous sinus and its surrounding regions. Incorporated with the petrous apectomy, it could be used to expose the petroclival region and, in selected cases, exposure could be extended to the convergence of the vertebral arteries. Combined with anterior and posterior clinoidectomies, it could also be used to treat midpoint regions of the basilar artery.

Basilar Artery↗
PubMed2001

Quantitative design of optimal analgesic combination of acetaminophen, caffeine, and butalbital.

AIM: To quantitatively seek an optimal analgesic combination of acetaminophen (Ace), butalbital (Bul), and caffeine (Caf), and to characterize the pharmacodynamics of interaction among the three drugs. METHODS: The models of acute inflammatory pain in carrageenin-injected rats were applied to measure the vocalization threshold to paw pressure. Six groups with different ratios and doses were set to seek an optimal combination of Ace, Caf, and Bul, analyzed by the weighted modification method. Based on the ratio and doses in the optimal combination, four continuous doses were set to analyze the interactions of therapeutic effects by the reflection method. The interaction of the acute toxicity was evaluated by the parameter method. RESULTS: According to the degree of importance to the combined analgesic effect, Ace > Caf > Bul; Ace showed a significant dose-response relationship, whereas in Caf and Bul, this relationship was not apparent. A new combination was obtained by the theoretical analysis and confirmed further by experimentation. Namely, at a ratio of 8.6:1:1.5 Ace + Caf + Bul (240 + 28 + 42 mg/kg, ig) was an optimal combination. Both Caf and Bul had a synergism to Ace, but Caf was a stronger synergist in contrast to Bul. Such synergism increased the therapeutic effects in the range of Ace 153.6 - 300 mg/kg combined with Caf 17.9 - 35 mg/kg and Bul 26.8 -5 2.5 mg/kg (8.6:1:1.5). However, the dose of Ace + Caf + Bul at 300 + 35 + 52.5 mg/kg resulted in sedation in rats. The peak latency was approximately 1 h for all four continuous doses, but the peak amplitude was dose-related, and the duration of the therapeutic effect was less than 2 h. The acute toxicity of the three drugs in combination remained the same. CONCLUSION: Ace + Caf + Bul at a dose of (240 + 28 + 42) mg/kg (ig) results in an optimal combination. The therapeutic window of the combination is located in the range of Ace (153.6 - 240 mg/kg)+Caf (17.9 - 28 mg/kg)+Bul (26.8 - 42 mg/kg) (8.6:1:1.5). Caf has a stronger synergism with Ace than Bul.

Acetaminophen↗
PubMed2001

[Telomerase activity inhibition and apoptosis induction of BEL-7404 human hepatoma cells by antisense oligonucleotides to telomerase RNA component].

Telomerase activity was detected in all of four human hepatoma cells but absent in normal liver tissue. Telomerase activity of BEL-7404 human hepatoma cells was inhibited effectively by antisense oligonucleotide to telomerase RNA component at final concentration of 1 mumol/L, whereas sense and missense oligonucleotides have no effects on its activity. The inhibition of telomerase activity was weakened, as the concentration of antisense oligonucleotide decreased. Treating BEL-7404 human hepatoma cells 96 hours continuously by the antisense oligomers at final concentration of 5 mumol/L, the morphology of treated cells changed and apoptosis percent of the cells increased markedly.

Apoptosis↗
PubMed2000

Identification of a functional domain in a GADD45-mediated G2/M checkpoint.

Cell cycle checkpoints are essential for the maintenance of genomic stability in response to DNA damage. We demonstrated recently that GADD45, a DNA damage-inducible protein, activates a G(2)/M checkpoint induced by either UV radiation or alkylating agents. GADD45 can interact in vivo with the G(2) cell cycle-specific kinase, Cdc2, proliferating cell nuclear antigen (PCNA), and the cell cycle kinase inhibitor p21(waf1). The ability of GADD45 to induce a G(2)/M arrest may be caused in part by the inhibition of Cdc2 kinase activity. Here, we report the identification of a region of GADD45 that is involved in this G(2)/M checkpoint. Mutants of GADD45 that lacked either the first 35 or the last 80 residues still retained an ability to induce G(2)/M arrest. A mutant with a deletion of the central region (residues 50-76), which is conserved in the family members GADD45beta and GADD45gamma, lacked such activity. This mutant also lacked an ability to bind to Cdc2, PCNA, and p21(waf1) in vivo. Consistently, either GADD45beta or GADD45gamma bind to Cdc2 in vivo. However, unlike GADD45, neither GADD45beta nor GADD45gamma inhibited the Cdc2 kinase or induced G(2)/M arrest. The unique effect of GADD45 may be caused by the presence of a region containing DEDDDR residues. Alanine substitutions in the region abolished GADD45 induction of a G(2)/M arrest and its inactivation of the Cdc2 kinase but not its binding to Cdc2, PCNA, or p21(waf1). Therefore, the binding of GADD45 to Cdc2 was insufficient to induce a G(2)/M arrest, and additional activity contributed by the DEDDDR residues may be necessary to regulate the G(2)/M checkpoint.

Amino Acid Sequence↗
PubMed2000

The RGG domain in hnRNP A2 affects subcellular localization.

The heterogeneous nuclear ribonucleoproteins (hnRNP) associate with pre-mRNA in the nucleus and play an important role in RNA processing and splice site selection. In addition, hnRNP A proteins function in the export of mRNA to the cytoplasm. Although the hnRNP A proteins are predominantly nuclear, hnRNP A1 shuttles rapidly between the nucleus and the cytoplasm. HnRNP A2, whose cytoplasmic overexpression has been identified as an early biomarker of lung cancer, has been less well studied. Cytosolic hnRNP A2 overexpression has also been noted in brain tumors, in which it has been correlated with translational repression of Glucose Transporter-1 expression. We now examine the role of arginine methylation on the nucleocytoplasmic localization of hnRNP A2 in the HEK-293 and NIH-3T3 mammalian cell lines. Treatment of either cell line with the methyltransferase inhibitor adenosine dialdehyde dramatically shifts hnRNP A2 localization from the nuclear to the cytoplasmic compartment, as shown both by immunoblotting and by immunocytochemistry. In vitro radiolabeling with [(3)H]AdoMet of GST-tagged hnRNP A2 RGG mutants, using recombinant protein arginine methyltransferase (PRMT1), shows (i) that hnRNP A2 is a substrate for PRMT1 and (ii) that methylated residues are found only in the RGG domain. Deletion of the RGG domain (R191-G253) of hnRNP A2 results in a cytoplasmic localization phenotype, detected both by immunoblotting and by immunocytochemistry. These studies indicate that the RGG domain of hnRNP A2 contains sequences critical for cellular localization of the protein. The data suggest that hnRNP A2 may contain a novel nuclear localization sequence, regulated by arginine methylation, that lies in the R191-G253 region and may function independently of the M9 transportin-1-binding region in hnRNP A2.

3T3 Cells↗
PubMed2000

Propofol directly depresses lumbar dorsal horn neuronal responses to noxious stimulation in goats.

PURPOSE: We tested the hypothesis that propofol, acting in the brain, would either enhance, or have no effect, on lumbar dorsal horn neuronal responses to a noxious mechanical stimulus applied to the hindlimb. We recorded the response of lumbar dorsal horn neurons during differential delivery of propofol to the brain and torso of goats. METHODS: Goats were anesthetized with isoflurane and neck dissections performed which permitted cranial bypass. A laminectomy was made to allow microelectrode recording of lumbar dorsal horn neuronal activity. Isoflurane was maintained at 0.8+/-0.1% to both head and torso throughout the study. During cranial bypass propofol was separately administered to the torso (1 mg x kg(-1), n = 7; 3.75 mg x kg(-1), n = 8) or cranial (0.04 mg x kg(-1), n = 7; 0.14 mg kg(-1), n = 8) circulations. RESULTS: Propofol administered to the torso depressed dorsal horn neuronal responses to noxious stimulation: low dose: 500+/-243 to 174+/-240 impulses x min(-1) at one minute post-injection, P<0.001; high dose: 478+/-204 to 91+/-138 impulses x min(-1) at one minute post-injection, P<0.05). Propofol administered to the cranial circulation had no effect: low dose: 315+/-150 to 410+/-272 impulses x min(-1), P>0.05; high dose: 462+/-261 to 371+/-196 impulses x min(-1), P>0.05. CONCLUSIONS: These data indicate that propofol has a direct depressant effect on dorsal horn neuronal responses to noxious stimulation, with little or no indirect supraspinal effect.

Analysis of Variance↗
PubMed2000

Isoflurane anaesthetic depth in goats monitored using the bispectral index of the electroencephalogram.

The bispectral index (BIS) of the electroencephalogram has recently been used to monitor the depth of anaesthesia in humans. The BIS is a dimensionless number that varies between 0 and 100. We hypothesized that the BIS could also be used to monitor depth of isoflurane anaesthesia in goats. Needle electrodes were placed over the frontal region of the scalp of goats and 5%, isoflurane was administered via a mask. The BIS number was determined at clinically relevant end-points. The BIS number did not change when the animals became recumbent (95 +/- 5 to 94 +/- 7, n = 15), but decreased to 65 +/- 13 and 64 +/- 15 when the corneal reflex and withdrawal response to a noxious stimulus, respectively, were lost (p < 0.001, n = 12). Direct laryngoscopy and intubation increased the BIS (56 +/- 7 to 83 +/- 11; p < 0.05, n = 10), as did a noxious pinch to the dew-claw (57 +/- 9; to 76 +/- 9; p < 0.05, n = 10). The spectral edge (frequency below which 95% of the total power resided) paralleled the change in BIS. We conclude that the depth of isoflurane anaesthesia in goats can be monitored using the BIS, although further work is needed to determine its sensitivity and specificity.

Anesthesia↗
PubMed2000

Using a non-radioisotopic, quantitative TRAP-based method detecting telomerase activities in human hepatoma cells.

A non-radioisotopic, quantitative TRAP-based telomerase activity assay was established mainly by using SYBR Green-I staining instead of radioisotope. Comparing with conventional radioisotope based method, it was better in reproducibility and accuracy. Using this method, we found telomerase activities were absent in normal human liver cells, while detected in all of four human hepatoma cell lines (BEL-7404, SMMC-7721, QGY-7903 and HCCM) without significant differences.

Animals↗
PubMed2000

Interaction of the PA2G4 (EBP1) protein with ErbB-3 and regulation of this binding by heregulin.

The processes by which ErbB-3, an inactive tyrosine kinase, exerts its biological effects are poorly understood. Using the yeast two-hybrid system, we have isolated an ErbB-3 binding protein (Ebp1) that interacts with the juxtamembrane domain of ErbB-3. This protein is identical to that predicted to be encoded for by the human PA2G4 gene. Ebp1 is the human homologue of a previously identified cell cycle-regulated mouse protein p38-2G4. Two transcripts of ebp1 mRNA (1.7 and 2.2 kb) were detected in several normal human organs. The interaction of Ebp1 with ErbB-3 was examined in vitro and in vivo. The first 15 amino acids of the juxtamembrane domain of ErbB-3 were essential for Ebp1 binding in vitro. Treatment of AU565 cells with the ErbB-3 ligand heregulin resulted in dissociation of Ebp1 from ErbB-3. Ebp1 translocated from the cytoplasm into the nucleus following heregulin stimulation. These findings suggest that Ebp1 may be a downstream member of an ErbB-3-regulated signal transduction pathway.

Animals↗
PubMed2000

Isoflurane action in the spinal cord blunts electroencephalographic and thalamic-reticular formation responses to noxious stimulation in goats.

BACKGROUND: Isoflurane depresses the electroencephalographic (EEG) activity and exerts part of its anesthetic effect in the spinal cord. The authors hypothesized that isoflurane would indirectly depress the EEG and subcortical response to noxious stimulation in part by a spinal cord action. METHODS: Depth electrodes were inserted into the midbrain reticular formation (MRF) and thalamus of six of seven isoflurane-anesthetized goats, and needle-electrodes were placed into the skull periosteum. In five of seven goats, an MRF microelectrode recorded single-unit activity. The jugular veins and carotid arteries were isolated to permit cranial bypass and differential isoflurane delivery. A noxious mechanical stimulus (1 min) was applied to a forelimb dewclaw at each of two cranial-torso isoflurane combinations: 1.1+/-0.3%-1.2+/-0.3% and 1.1+/-0.3-0.3+/-0.1% (mean +/- SD). RESULTS: When cranial-torso isoflurane was 1.1-1.2%, the noxious stimulus did not alter the EEG. When torso isoflurane was decreased to 0.3%, the noxious stimulus activated the MRF, thalamic, and bifrontal-hemispheric regions (decreased high-amplitude, low-frequency power). For all channels combined, total (-33+/-15%), delta(-51+/-22%), theta (-33+/-19%), and alpha (-26+/-16%) power decreased after the noxious stimulus (P<0.05); beta power was unchanged. The MRF unit responses to the noxious stimulus were significantly higher when the spinal cord isoflurane concentration was 0.3% (1,286+/-1,317 impulses/min) as compared with 1.2% (489+/-437 impulses/min, P<0.05). CONCLUSIONS: Isoflurane blunted the EEG and MRF-thalamic response to noxious stimulation in part via an action in the spinal cord.

Anesthetics, Inhalation↗
PubMed2000

Anti-hepatoma activity of taxol in vitro.

AIM: To investigate the in vitro anti-hepatoma activity of taxol against SMMC-7721 human hepatoma cells. METHODS: The hepatoma cell growth was measured by MTT-microculture tetrazolium assay. Cell-cycle kinetics and apoptosis were analyzed by flow cytometry and microscopic examination. RESULTS: Taxol inhibited the hepatoma cell growth in concentration- and time-dependent manners with IC50 of 18.96 nmol.L-1. Marked cell accumulation in G2/M phase and multinucleated cells were also observed after treatment with taxol 10 nmol.L-1. In addition, taxol at 10 nmol.L-1 could induce the apoptosis of hepatoma cells. CONCLUSION: Taxol suppresses the growth of SMMC-7721 human hepatoma cells in vitro by causing cell-cycle arrest, aberrant mitosis, and apoptosis of the human hepatoma cells.

Antineoplastic Agents, Phytogenic↗
PubMed2000

Human hepatoma cell telomerase activity inhibition and cell cycle modulation by its RNA component antisense oligodeoxyribonucleotides.

AIM: To investigate the effects of human telomerase RNA component antisense oligodeoxyribonucleotides on telomerase activity of human hepatoma cells and their effects on cell cycle distribution. METHODS: Modified telomeric repeat amplification protocol was used to detect telomerase activity. Cell cycle was analyzed by flow cytometer. RESULTS: Telomerase activity was detected in all of four human hepatoma cell lines but absent in normal liver cells. Antisense oligomers to human telomerase RNA component (hTR) inhibited telomerase activity of BEL-7404 human hepatoma cells markedly in vitro. After in vitro treatment with antisense oligomers for 96 h, cell cycle of BEL-7404 human hepatoma cells was mainly arrested at G2/M phase. CONCLUSION: Antisense oligomers to hTR inhibited telomerase activity of BEL-7404 human hepatoma cells in vitro and resulted in cell cycle arrest at G2/M phase.

Carcinoma, Hepatocellular↗
PubMed2000

[The retrosigmoid approach surgery of trigeminal never].

OBJECTIVE: To explore the effect of retrosigmoid approach surgery of trigeminal never to treat trigeminal neuralgia. METHOD: Twenty-six patients underwent the selective trigeminal neurectomy, among them 2 cases of surgical removal of the cerebellopontine angle cholesteatoma and 2 cases of trigeminal never branch No. I splitting; four patients underwent microvascular decompression. RESULT: By 1-7 years of following up, only one case of microvascular decompression recurrence in all successful operations. CONCLUSION: The effect of retrosigmoid approach surgery of trigeminal never is satisfactory. To know the management of the complications is very important too.

Adult↗
PubMed2000

[Determination of sialic acids in serum of lung cancer with ultrafiltration-capillary electrophoresis].

A method for the determination of sialic acids in serum with ultrafiltration-capillary electrophoresis is described and the operation was optimized. Sialic acids were directly separated and analyzed with UV detection at 195 nm and without pre-or post-column derivatization. The recovery of N-acetylneuraminic acid (NANA) was 92.6%, the concentration and mass detection limit of NANA were 9.6 mumol/L and 39 fmol respectively. This method was used for the determination of NANA level in the serum of 11 lung cancer patients and 30 normal adults. The results showed that the average concentration of NANA in the serum of patients was much higher than that of normal adults with P < 0.001. The results were also compared with those obtained by the traditional colorimetric method, with good linear relationship of r = 0.983 at n = 10. It is concluded that the method described in this paper is simple and sensitive, and is suitable for basic research and clinical applications to malignant tumors.

Adult↗
PubMed1999

Preferential binding of tumor suppressor p53 to positively or negatively supercoiled DNA involves the C-terminal domain.

The C-terminal domain of the tumor suppressor protein p53 is the site of non-specific DNA binding. Purified p53 produced from baculovirus-infected insect cells binds preferentially to supercoiled DNA, forming bands with lower electrophoretic mobility. This non-covalent binding does not change the linking number of the DNA. An anti-p53 antibody targeting the C-terminal domain partially competes with supercoiled DNA in binding to p53, while antibodies targeted to the N terminus of p53 supershift the complex bands. A synthetic peptide corresponding to amino acid residues 319-393 of human p53 also displays preferential binding to supercoiled DNA, while a mutant peptide, which is unable to form tetramers, is inactive. The center of the equilibrium distribution of topoisomers formed by relaxation with topoisomerase I is not shifted in the presence of p53 although the distribution is broadened. The preferential binding of p53 is exhibited toward both positively and negatively supercoiled DNA. These observations are consistent with a model in which p53 binds to right-handed or left-handed strand crossings.

Antibodies↗
PubMed1999

Characterization and chromosomal localization of USP3, a novel human ubiquitin-specific protease.

Conjugation to the small eukaryotic protein ubiquitin can functionally modify or target proteins for degradation by the proteasome. Removal of the ubiquitin modification, or deubiquitination, is performed by ubiquitin-specific proteases and is an important mechanism regulating this pathway. Here we describe a novel human ubiquitin-specific protease, USP3, initially identified as a partial cDNA clone similar to one of two highly conserved sequence regions common to all ubiquitin-specific proteases. We have isolated a complete USP3 cDNA clone containing both of these conserved sequence regions. The USP3 gene appears to be single copy and maps to human chromosome 15q22.3. A USP3 probe detects two mRNA transcripts, one of which corresponds in length to the cDNA. Both are expressed at low levels in all tissues examined, with highest expression in pancreas. The USP3 protein is a functional ubiquitin-specific protease in vitro, and is able to inhibit ubiquitin-dependent degradation of both an N-end Rule substrate and abnormal endogenous proteins in yeast. USP3 is also only the second known ubiquitin-specific protease capable of efficiently cleaving a ubiquitin-proline bond.

Alternative Splicing↗
PubMed1999

Drug-induced apoptosis is delayed and reduced in XPD lymphoblastoid cell lines: possible role of TFIIH in p53-mediated apoptotic cell death.

The tumor suppressor gene product p53 can bind to and inhibit the helicase activity of the multisubunit transcription-repair factor TFIIH. We previously reported that p53-mediated apoptosis is attenuated in primary human fibroblasts from individuals with Xeroderma Pigmentosum (XP) that harbor mutations in the TFIIH DNA helicases XPD or XPB. In this study we show that apoptosis is reduced and delayed in three XPD lymphoblastoid cell lines (LCLs), but not in an XPD heterozygote LCL, after exposure to doxorubicin, a DNA-damaging agent and topoisomerase II inhibitor frequently used in cancer therapy. Apoptosis was assessed by quantitation of Annexin V binding to exposed phosphatidylserine residues and by caspase-mediated cleavage of Poly(ADP)Ribose Polymerase (PARP). Apoptosis induced by doxorubicin was suppressed in LCLs retrovirally transduced with the Human Papillomavirus 16 E6 oncoprotein, consistent with the hypothesis that this is a p53-dependent process. PARP cleavage was not delayed in XPD LCLs in response to anti-Fas (CD95) antibody-mediated apoptosis, thus, the defect in the apoptotic pathway in these cells lies upstream of caspase activation. Similar changes in the expression of apoptosis-effector genes, p53, and p53-responsive genes p21Cip1/WAF-1/Sid1 (p21), gadd45, bcl-2 and bax were observed in normal and XPD LCLs after treatment with doxorubicin, indicating that delayed apoptosis was not a consequence of defective transcription of these genes. Thus, our studies provide further support to the hypothesis that XPD and p53 can functionally interact in a p53-mediated apoptotic pathway.

Antineoplastic Agents↗