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Biomedical subjects

G Cheng

Publications and source records attributed to G Cheng.

At least 91 records · Page 5Linked to original sources

Improvement in transfusion safety using a specially designed transfusion wristband.

Fatal haemolytic transfusion reaction due to ABO incompatibility occurs mainly as a result of clerical error. A blood sample drawn from the wrong patient and labelled as another patient's will not be detected by the blood bank unless there is a previous ABO grouping result. We report here the detection of such clerical error by the use of a specially designed transfusion wristband. The wristband has the following special features: (i) once attached, it cannot be removed except by cutting; (ii) it has a pocket containing a transfusion label; (iii) a unique transfusion barcode is printed on each transfusion label and the corresponding wristband simultaneously by computer technology; (iv) a transfusion label removed from the wristband after attachment to the patient has a characteristic tear-mark distinguishing it from one removed prior to attachment. The blood bank only accepted those specimens bearing the tear-marked transfusion labels. All blood units for this patient were labelled with this unique transfusion code together with the patient's details. The nurses counter-checked the transfusion code on the blood units against the transfusion code on the patient's transfusion wristband prior to transfusion. If the blood sample for compatibility testing was drawn from the 'wrong' patient, the intended patient either did not carry a wristband or the transfusion codes did not match at all. Pretransfusion compatibility tests were performed on 2189 patient samples using this procedure. It was well accepted by both ward and blood bank staff. Two potential mismatched transfusions were avoided. These two clerical errors would not have been detected because neither patient had previous ABO grouping results.

Blood Banks↗

Assessment of optic nerve compression in Graves' ophthalmopathy. The usefulness of a quick T1-weighted sequence.

PURPOSE: Diagnosis of optic nerve compression can be difficult in patients with equivocal clinical signs. We examined the usefulness of a quick coronal MR sequence performed at a predetermined plane as a screening tool for selecting patients at high risk of optic nerve compression. MATERIAL AND METHODS: Direct coronal images of the orbit were obtained in 37 patients with Graves' disease in a predetermined plane. The muscular indices (MI) of each orbit were calculated. Mann-Whitney U-Wilcoxon rank sum test was used to assess if there was any statistically significant difference between patients with and without signs of optic nerve compression. The ROC curve was used to identify a value useful for discriminating patients with a higher risk of developing optic nerve compression. RESULTS: There was a statistically significant difference (p<0.05) in the MI between patients with and without optic nerve compression. An MI of -0.48 had 100% sensitivity, 89% specificity and 91% accuracy in identifying patients with optic nerve compression. CONCLUSION. A quick coronal MR image obtained at the mid-orbital plane is useful in screening patients with Graves' disease for optic nerve compression.

Female↗

Enflurane directly depresses glutamate AMPA and NMDA currents in mouse spinal cord motor neurons independent of actions on GABAA or glycine receptors.

BACKGROUND: The spinal cord is an important anatomic site at which volatile agents act to prevent movement in response to a noxious stimulus. This study was designed to test the hypothesis that enflurane acts directly on motor neurons to inhibit excitatory synaptic transmission at glutamate receptors. METHODS: Whole-cell recordings were made in visually identified motor neurons in spinal cord slices from 1- to 4-day-old mice. Excitatory postsynaptic currents (EPSCs) or potentials (EPSPs) were evoked by electrical stimulation of the dorsal root entry area or dorsal horn. The EPSCs were isolated pharmacologically into glutamate N-methyl-d-aspartate (NMDA) receptor- and non-NMDA receptor-mediated components by using selective antagonists. Currents also were evoked by brief pulse pressure ejection of glutamate under various conditions of pharmacologic blockade. Enflurane was made up as a saturated stock solution and diluted in the superfusate; concentrations were measured using gas chromatography. RESULTS: Excitatory postsynaptic currents and EPSPs recorded from motor neurons by stimulation in the dorsal horn were mediated by glutamate receptors of both non-NMDA and NMDA subtypes. Enflurane at a general anesthetic concentration (one minimum alveolar anesthetic concentration) reversibly depressed EPSCs and EPSPs. Enflurane also depressed glutamate-evoked currents in the presence of tetrodotoxin (300 nm), showing that its actions are postsynaptic. Block of inhibitory gamma-aminobutyric acid A and glycine receptors by bicuculline (20 micrometer) or strychnine (2 micrometer) or both did not significantly reduce the effects of enflurane on glutamate-evoked currents. Enflurane also depressed glutamate-evoked currents if the inhibitory receptors were blocked and if either D,L-2-amino-5-phosphonopentanoic acid (50 micrometer) or 6-cyano-7-nitroquinoxaline-2,3-dione disodium (10 micrometer) was applied to block NMDA or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-kainate receptors respectively. CONCLUSIONS: Enflurane exerts direct depressant effects on both alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and NMDA glutamate currents in motor neurons. Enhancement of gamma-aminobutyric acid A and glycine inhibition is not needed for this effect. Direct depression of glutamatergic excitatory transmission by a postsynaptic action on motor neurons thus may contribute to general anesthesia as defined by immobility in response to a noxious stimulus.

2-Amino-5-phosphonovalerate↗

Induction of apoptotic cell death in peripheral blood mononuclear and polymorphonuclear cells by an oral bacterium, Fusobacterium nucleatum.

It is largely unknown why a variety of bacteria present in the oral cavity are capable of establishing themselves in the periodontal pockets of nonimmunocompromised individuals in the presence of competent immune effector cells. In this paper we present evidence for the immunosuppressive role of Fusobacterium nucleatum, a gram-negative oral bacterium which plays an important role in the generation of periodontal disease. Our studies indicate that the immunosuppressive role of F. nucleatum is largely due to the ability of this organism to induce apoptotic cell death in peripheral blood mononuclear cells (PBMCs) and in polymorphonuclear cells (PMNs). F. nucleatum treatment induced apoptosis of PBMCs and PMNs as assessed by an increase in subdiploid DNA content determined by DNA fragmentation and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling assays. The ability of F. nucleatum to induce apoptosis was abolished by either heat treatment or proteinase digestion but was retained after formaldehyde treatment, suggesting that a heat-labile surface protein component is responsible for bacterium-mediated cell apoptosis. The data also indicated that F. nucleatum-induced cell apoptosis requires activation of caspases and is protected by NF-kappaB. Possible mechanisms of F. nucleatum's role in the pathogenesis of periodontal disease are discussed.

Apoptosis↗

Effects of aging on surfactant forms in rats.

Surfactant present in the alveolar space exists in two major forms: functional large aggregate forms (LA) and nonfunctional small aggregate forms (SA), but there is no information about the changes of surfactant forms and the rate of conversion of LA to SA in the aged lungs. The purpose of the present study was to investigate the developmental aspects of surfactant forms in newborn, young, middle-aged and aged rats, LA and SA were recovered from alveolar lavages of rats. The rate of conversion from LA to SA was then analysed using a surface-area cycling technique. Age-related changes of saturated phosphatidylcholine (Sat-PC) and surfactant protein A (SP-A) pool sizes were also evaluated in alveolar lavages. The alveolar lavages recovered from aged rats contained a significantly higher proportion of LA than did those obtained from young or newborn rats. There was also an age-related decrease in the rate of conversion from LA to SA in vitro. The Sat-PC pool sizes in the alveolar lavages decreased with age, but the SP-A contents were similar between young and aged rats. These results suggested that decreased form conversion may contribute to maintaining functional surfactant pool sizes in the lungs of aged rats.

Aging↗

Increased levels of surfactant protein A and D in bronchoalveolar lavage fluids in patients with bronchial asthma.

Surfactant proteins (SP)-A and SP-D are collagen-like glycoproteins belonging to the "collectin" class of C-type lectins, which are primarily synthesized in type II cells. Recent studies reported the possibility of local production of SP-A and SP-D in the airways, but the amounts of surfactant proteins in patients with bronchial asthma have not been studied. The composition of surfactant proteins in mild, stable asthmatics in the first lavage as bronchial lavage (BL) and the second and third lavages consecutively as alveolar lavages (AL) were therefore, analysed separately. The co-relationships in the BL between the amounts of surfactant proteins and those of fucose, which is one of the markers of submucosal secretion were also analysed. Increased amounts of SP-A in BL and AL of in asthmatics were found as compared with those in controls. A high concentration of SP-D in the AL asthma patients was also found. The levels of SP-A correlated with those of fucose in patients with bronchial asthma (r=0.849, p<0.01). The observations in the present study suggested that surfactant protein A may be secreted from the airways with allergic inflammation in a different manner from the alveoli. The increased levels of surfactant proteins A and D may play a protective role in an allergic inflammation in the pathogenesis of bronchial asthma.

Adult↗

Neuroprotective role for the p50 subunit of NF-kappaB in an experimental model of Huntington's disease.

Prototypical NF-kappaB consists of a transcription factor dimer of p50 and p65, and an inhibitory subunit called I-kappaB. NF-kappaB is activated in neurons in response to excitotoxic, metabolic, and oxidative stress. Cell-culture data suggest that activation of NF-kappaB can prevent neuronal apoptosis, but its role in vivo is unclear and the specific kappaB subunits involved are unknown. In Huntington's disease (HD), striatal neurons degenerate, and a similar pattern of neuronal vulnerability occurs in rats and mice following exposure to the mitochondrial toxin 3-nitropropionic acid (3NP). We report that mice lacking the p50 subunit of NF-kappaB exhibit increased damage to striatal neurons following administration of 3NP. The neuronal death occurs by apoptosis as indicated by increased caspase activation and DNA fragmentation into oligonucleosomes. NF-kappaB activity is markedly increased in striatum 24-72 h following 3NP administration in wild-type mice, but not in mice lacking p50, indicating that p50 is necessary for the vast majority of 3NP-induced NF-kappaB DNA-binding activity in striatum. Cultured striatal neurons from p50-/- mice exhibited enhanced oxidative stress, perturbed calcium regulation, and increased cell death following exposure to 3NP, suggesting a direct adverse effect of p50 deficiency in striatal neurons.

Animals↗

Pivotal role for acidic sphingomyelinase in cerebral ischemia-induced ceramide and cytokine production, and neuronal apoptosis.

Stroke is a major cause of long-term disability, the severity of which is directly related to the numbers of neurons that succumb to the ischemic insult. The signaling cascades activated by cerebral ischemia that may either promote or protect against neuronal death are not well understood. One injury-responsive signaling pathway that has recently been characterized in studies of non-neural cells involves cleavage of membrane sphingomyelin by acidic and/or neutral sphingomyelinase (ASMase) resulting in generation of the second messenger ceramide. We now report that transient focal cerebral ischemia induces large increases in ASMase activity, ceramide levels, and production of inflammatory cytokines in wild-type mice, but not in mice lacking ASMase. The extent of brain tissue damage is decreased and behavioral outcome improved in mice lacking ASMase. Neurons lacking ASMase exhibit decreased vulnerability to excitotoxicity and hypoxia, which is associated with decreased levels of intracellular calcium and oxyradicals. Treatment of mice with a drug that inhibits ASMase activity and ceramide production reduces ischemic neuronal injury and improves behavioral outcome, suggesting that drugs that inhibit this signaling pathway may prove beneficial in stroke patients.

Animals↗

[Analyzing study of complications of tissue expansion related to the injectable system].

OBJECTIVE: To analyze the complications of tissue expansion related to its injectable system. METHODS: One hundred and ninety six patients were followed up and analyzed for the complications of the tissue expansion concerned to its injectable system. The management of these complications was also reviewed. RESULTS: There were five kinds of the complications(with the occurrence of 32%) related to the injectable system in this group patients. The highest frequency of the complications occurred in the implantation stage. Further management was also documented well. CONCLUSION: The complications of tissue expansion related to the injectable system occurred commonly and should be paid more attention on them.

Adolescent↗

[hCG-PLZF-RARA transgenic mice develop leukemia resembling human chronic myeloid leukemia].

OBJECTIVE: In order to investigate the leukemogenic potential of PLZF-RARA fusion protein in vivo, hCG-PLZF-RARA transgenic mice were generated, in which PIZF-RARA fusion gene was driven by hCG promoter to express in myeloid cells of mice. METHODS: Molecular cloning technology was used to construct hCG-PLZF-RARA gene. The genotype and phenotype of the hCG-PLZF-RARA transgenic mice were analyzed by PCR, RT-PCR, immunofluorescence, morphology of bone marrow (BM) cells, pathology and retinoic acid differentiation assays. RESULTS: Six hCG-PLZF-RARA transgenic mice developed leukemia resembling human chronic myeloid leukemia. TF(tissue factor) was not expressed in BM cells of normal mice nor in mice without the expressed transgene, but it was expressed in mice expessing the transgene. CONCLUSION: PLZF-RARA fusion protein plays a crucial role in leukemogenesis. TF is up-regulated by PLZF-RARA fusion gene.

Animals↗

[The selection of taxol resistance associated genes in ovarian cancer cell line by mRNA DD].

OBJECTIVE: One of the main reasons of the treatment failure for ovarian cancer is the emergence of drug resistance in which several genes involved. The purpose of the study was to select the genes related to Taxol resistance in ovarian cancer. METHODS: Resistant ovarian cancer cell line, Skov3/Taxol-25, was established by interval exposure Skov3 to Taxol. mRNA was compared between Skov3 and Skov3/Taxol-25 by mRNA DD. RESULTS: Skov3/Taxol-25 showed 44 times increase resistance to Taxol after 12 months of induction. There were 22 new differential bands obtained from Skov3/Taxol-25 as compared with Skov3. 18 bands were special by repeated PCR. In the 5 sub-clones, three clones were homologous to the known gene. 105/106 base pair of clone 1 were homologous to tPA (tissue plasminogen activator), 261/268 of clone 3 to Kiaa 0372, and 406/409 of clone 18 to LDLC. The other 2 ESTs were new gene segments, which were banked to Genbank with the number of AF120327 and AF120328. The identification by RT-PCR revealed that both tPA and Kiaa0372 were special genes from Skov3/Taxol-25, while LDLC was pseudopositive. CONCLUSION: Several genes were involved in the resistance to Taxol in ovarian cancer. The enhanced expression of tPA indicated the increased ability of metastasis after the acquisition of resistance to taxol.

Antineoplastic Agents, Phytogenic↗

[The expression of multiple drug resistance associated genes in ovarian cancer].

OBJECTIVE: The aim of the investigation was to find out the relationship between the expression of multidrug resistance gene (MDR1), multidrug resistance protein (MRP), lung resistance protein (LRP) and glutathione S-transferase pi (GST-pi) with the clinical pathological characteristics and the prognosis in the ovarian cancer patients who never received chemotherapy before operation. METHODS: The expression of MDR1, MRP, LRP and GST-pi in 41 cases of ovarian cancer, 25 cases of benign ovarian tumor and 12 normal ovary tissue were investigated by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: In normal ovary, benign tumor and ovarian cancer, the positive expression of MDR1 was 0.0%, 0.0% and 29.3%, the positive of MRP was 16.7%, 12.0% and 53.7%, the positive of LRP was 25.0%, 52.0% and 87.8%, the positive of GST-pi was 8.3%, 12.0% and 51.2% respectively. The ratios of co-expression of multiple genes in ovarian cancer were much higher than that in benign ovarian tumor. All tested genes showed no significant relationship to the clinical stage, histological type and the differentiation of the tumor except that the expression of MDR1 and MRP was closely related to the differentiation (P < 0.05). The non-responders to platinum or taxol based combination chemotherapy exhibited higher ratios of MDR1 and MRP expression than the responders (P < 0.05). Furthermore, the co-expression phenomenon was more common in non-responders. CONCLUSIONS: Multiple gene expression is involved in drug resistance in ovarian cancer. The co-expression of MDR1, MRP, LRP and GST-pi is higher in ovarian cancer than that in benign ovarian tumor and normal ovary tissue. The expression of MDR1 and MRP is closely related to the tumor differentiation and the response to chemotherapy.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

[Advance in study of artificial nerve].

OBJECTIVE: To review the advance in materials of nerve conduit and Schwann cell transplantation for preparation of artificial nerve with tissue engineering technique. METHODS: Recent literatures about artificial nerve, nerve conduit and Schwann cell transplantation were extensively reviewed. RESULTS: Many biomaterials such as silicon, dacron, expanded polytetrafluoroethylene(ePTFE), polyester and chitin could be used as nerve conduits to repair nerve defect, the degradable biomaterials were better. The nerve conduit with intrinsic filaments could be used to bridge an extended gap in peripheral nerve. Purified and cultured Schwann cells were still bioactive. Axonal regeneration could be enhanced after implantation of Schwann cells into nerve conduit. CONCLUSION: The ideal artificial nerve is composed of three dimensional biodegradable nerve conduit and bioactive Schwann cells, Schwann cells can be distributed in nerve conduit just like Bünger's band.

Biocompatible Materials↗

Ethanol reduces neuronal excitability and excitatory synaptic transmission in the developing rat spinal cord.

Effects of acute ethanol (EtOH) exposure on motoneuron excitability and properties of synaptic transmission were examined in spinal cords of postnatal rats. Whole-cell patch clamp recordings and intracellular recordings with high-resistance electrodes were carried out in motoneurons of 1- to 4-day-old postnatal rats. To determine the effects of extracellular EtOH on action potential waveform, properties of current-evoked soma action potentials and motoneuron ability to generate repetitive action potential firing were examined. During a brief EtOH (70 mM) exposure, larger depolarizing current was required for action potential generation, the duration of the after hyperpolarizing potential increased, and fewer action potentials were produced during a prolonged intracellular current injection. These effects were reversed within 20 min of EtOH removal from the extracellular solution. To determine whether the reduced probability of action potential generation was associated with changes in synaptic transmission, properties of evoked synaptic potentials and spontaneous synaptic currents were investigated. In the presence of EtOH, the amplitude of dorsal root-evoked synaptic potentials was reduced, the frequency of spontaneous excitatory postsynaptic currents decreased, while the frequency of inhibitory postsynaptic currents increased. Our data suggested that acute EtOH exposure suppressed motoneuron electrical activity by decreasing motoneuron excitability and shifting the balance between excitatory and inhibitory synaptic transmission toward inhibition.

Action Potentials↗

NF-kappaB-mediated up-regulation of Bcl-x and Bfl-1/A1 is required for CD40 survival signaling in B lymphocytes.

Activation of CD40 is essential for thymus-dependent humoral immune responses and rescuing B cells from apoptosis. Many of the effects of CD40 are believed to be achieved through altered gene expression. In addition to Bcl-x, a known CD40-regulated antiapoptotic molecule, we identified a related antiapoptotic molecule, A1/Bfl-1, as a CD40-inducible gene. Inhibition of the NF-kappaB pathway by overexpression of a dominant-active inhibitor of NF-kappaB abolished CD40-induced up-regulation of both the Bfl-1 and Bcl-x genes and also eliminated the ability of CD40 to rescue Fas-induced cell death. Within the upstream promoter region of Bcl-x, a potential NF-kappaB-binding sequence was found to support NF-kappaB-dependent transcriptional activation. Furthermore, expression of physiological levels of Bcl-x protected B cells from Fas-mediated apoptosis in the absence of NF-kappaB signaling. Thus, our results suggest that CD40-mediated cell survival proceeds through NF-kappaB-dependent up-regulation of Bcl-2 family members.

Apoptosis↗

Ethanol inhibits L1-mediated neurite outgrowth in postnatal rat cerebellar granule cells.

The neuropathology of the effects of ethanol on the developing central nervous system are similar to those of patients with mutations in L1, a neural cell adhesion molecule. This observation suggests that inhibition of L1 plays a role in the pathogenesis of alcohol-related neurodevelopmental disorders. Here we examine the effects of ethanol on L1 homophilic binding and on L1-mediated neurite outgrowth. Ethanol had no effect on cell adhesion or aggregation in a myeloma cell line expressing full-length human L1. In contrast, the rate of L1-mediated neurite outgrowth of rat postnatal day 6 cerebellar granule cells grown on a substratum of NgCAM, the chick homologue of L1, was inhibited by 48.6% in the presence of ethanol with a half-maximal concentration of 4.7 mM. The same effect was found with soluble L1-Fc, thus showing that the inhibitory effect is not dependent on cell adhesion. In contrast, neither laminin nor N-cadherin-mediated neurite outgrowth was inhibited by physiologic concentrations of ethanol. We conclude that one mechanism of ethanol's toxicity to the developing central nervous system may be the inhibition of L1-mediated neurite outgrowth.

Animals↗

The role of GATA, CArG, E-box, and a novel element in the regulation of cardiac expression of the Na+-Ca2+ exchanger gene.

The cardiac Na+-Ca2+ exchanger (NCX1) is the principal Ca2+ efflux mechanism in cardiocytes. The exchanger is up-regulated in both cardiac hypertrophy and failure. In this report, we identify the cis-acting elements that control cardiac expression and alpha-adrenergic up-regulation of the exchanger gene. Deletion analysis revealed that a minimal cardiac promoter fragment from -184 to +172 is sufficient for cardiac expression and alpha-adrenergic stimulation. Mutational analysis revealed that both the CArG element at -80 and the GATA element at -50 were required for cardiac expression. Gel mobility shift assay supershift analysis demonstrated that the serum response factor binds to the CArG element and GATA-4 binds to the GATA element. Point mutations in the -172 E-box demonstrated that it was required for alpha-adrenergic induction. In addition, deletion analysis revealed one or more enhancer elements in the first intron (+103 to +134) that are essential for phenylephrine up-regulation but bear no homology to any known transcription element. Therefore, this work demonstrates that SRF and GATA-4 are critical for NCX1 expression in neonatal cardiomyocytes and that the -172 E-box in addition to a novel enhancer element(s) are required for phenylephrine up-regulation of NCX1 and may mediate its hypertrophic up-regulation.

Adrenergic alpha-Agonists↗