Biomedical subjects
Publications and source records attributed to Y Lu.
OBJECTIVE: To set up a method for analyzing and distinguishing all the chemical components in natural Caoulus Bovis. METHOD: Powder X-ray diffraction analyses was used to analyze four samples of natural Caculus Bovis, and the X-ray diffraction Fourier pattern was obtained for distinguishing natural Caculus Bovis. RESULT AND CONCLUSION: The method can be used for distinguishing animal medicinal materials.
In this study, four metal porphyrins (tetraphenylporphyrinesulfonatoiron, tetraphenylporphyrinesulfon-atocopper, tetraphenylporphyrinesulfonatomanganese, and tetraphenyl porrphyrinesulfonatocobalt) were used as dual function mimicry of superoxide dismutase (SOD) and catalase (CAT). The first function, scavenging O2.-, has been proved by using riboflavine-methionine photoreduction method in the concentration range of 10(-5)-10(-6) mol/L. The second function, scavenging H2O2, has been demonstrated by means of spectrophotometry, and the percentage of decomposing H2O2 increases with the concentration of the imitating compounds. Metal porphyrins, SOD and CAT were measured by the liver homogenate technique of mice and the results showed that they had obvious action of decreasing the lipid peroxidation. Tetraphenylporphyrinesulfonatomanganese was measured by isolated ischemia reperfusion heart of rats. The results indicated that the Mn-TPPS4 could reduce the damages of active oxygen and had evidently protective effects on isolated ischemia-reperfusion mocardium of rats.
For the detection of Neisseria gonorrhoeae(NG), Chlamydia trachomat is(CT) and Ureaplasma urealyticum(UU) in urogenital infection in one specimen, multiple primer PCR was used in 156 sex transmitted disease patients, it was shown that in 156 specimens there were 40 NG positive and 31 CT positive and 27 UU positive, 10 NG + CT positive, 4 NG + UU positive, 3 CT + UU positive and 2 NG + CT + UU positive respectively. The results were in correspondence with each other. It is suggested that multiple primer PCR is a quick, sensitive, simple and specific technique which can be applied in clinical test.
A 1.1 bp fragment of E2 gene of Chinese classical swine fever virus(CSFV) Shimen strain, a standard virulent strain, was amplified by RT-PCR from total RNA of cell cultures infected by CSFV, and cloned into pGEM T vector. The nucleotide sequence of this fragment was sequenced by Sanger's method and the amino acid sequence was deduced. Compared with the corresponding region of Alfort, Brescia and C strain of CSFV, the nucleotide sequence homology is 84.7%, 92.6% and 95.2% respectively, and the amino acid sequence 89.4%, 92.6% and 94.6%, respectively, we subcloned 1.1 bp of E2 gene cDNA into baculovirus transfer vector and successfully constructed two recombinant baculoviruses expressing GST-E2 and GST-GFP-E2 fusion protein respectively by homologous recombination in sf-9 cell. Furthermore, we also constructed recombinant eukaryotic expression vector pcE2 containing E2 gene in frame and transfected COS-7 cell by lipofectamine, the indirect immunofluorescence assay (IFA) showed that the expressed E2 protein can be recognized by E2 specific monoclonal antibody the pcE2 DNA was directly injected into BALB/c mice intramuscular(i.m.) and the CSFV E2-specific antibodies was measured by enzyme-linked immunosorbent assay(ELISA) the ELISA results indicated the E2-specific antibodies was induced in inoculated mice and virus neutralization assays also indicate single inoculations of plasmids expressing CSFV E2 glycoprotein raised neutralizing antibody in BALB/c mice. these results will be beneficial to investigate the possibility of DNA vaccine against CSFV.
PURPOSE: To explore the toxicity of Mitomycin C (MMC) on trabecular meshwork cells. METHODS: Bovine trabecular meshwork cells were cultured in vitro and exposed to MMC of different concentrations. The cellular morphology, ultrastructure, mortality and phagocytosis was studied with light microscopy, transmission electron microscopy and methods of Wright's stain, etc. RESULTS: It was found that the toxic effect of MMC on the cells was in a dose-dependent mode. 1 x 10(-2) and 1 x 10(-3) mg/ml of MMC caused a large part of cells dead, 1 x 10(-4) and 1 x 10(-5) mg/ml of the drug had remarkable killing effect on the cells. 1 x 10(-6) mg/ml of MMC had still a mild toxicity, while 1 x 10(-7) mg/ml of MMC had not any influence on cellular morphology, mortality, and phagocytosis, etc. The safe concentration on bovine trabecular meshwork cells was 1 x 10(-7) mg/ml and the LD50 was between 1 x 10(-3) and 1 x 10(-4) mg/ml. CONCLUSIONS: Refering to previous data, we conclude that conventional clinical-application of MMC might do harm to trabecular meshwork cells.
OBJECTIVE: To evaluate the hearing function in patients with hereditary progressive non-syndromic hearing loss. METHODS: Distortion product otoacoustic emissions (DPOAE) and pure tone audiometry were carried out in 52 individuals from a family with non-syndromic hearing loss and 15 persons with normal hearing. RESULTS: 1. Sensorineural hearing loss (SNHL) was found in 34 individuals of the family. Among these individuals, DPOAE was totally absent in 15 cases (29 ears) with pure tone average > or = 40 dB and low amplitude or absent middle to high frequencies in 12 cases (23 ears) with high frequency hearing loss but pure tone average < or = 35 dB. 2. Among 21 individuals (42 ears) with normal audiograms, DPOAE presented lower amplitude or absent high and middle frequencies in 12 individuals. CONCLUSION: DPOAE can be used in identification of subclinical pathologic alterations in the cochlea. This would be of particular value in early diagnosis and genetic consultation.
OBJECTIVE: The purpose of this study was to observe the distribution of Acetylcholine receptor (AchR) and ultrastructural changes of the neuromuscular junction after laryngeal reinnervation. METHODS: alpha-bungarotoxin-horseradish peroxidase (alpha-BT-HRP) conjugate electron microscopic immunocytochemical methods and computer analysis of intensity of immunocytochemical reaction were applied to observe the distribution and relative quantity of junctional N-AchR. RESULTS: The results showed that the synaptic nerve terminals and presynaptic membrane were segmentally disrupted and almost disappeared completely and were replaced by Schwann's cells at 3 weeks after neurorrhaphy. At 6 weeks, some of the regenerating axons grew to the neuromuscular junctions and all the muscle fibers were reinnervated at 12 weeks. But the original postsynaptic membranes were only partially in contact with the regenerated nerve terminals. These conditions persisted until 18 weeks after neurorrhaphy, when remyelination was found in the vicinity of the neuromuscular junctions. The N-AchR reaction product on the postsynaptic membrane were increased greatly about 1.28 times more than the normal at 3 weeks after neurorrhaphy. The reactive products decreased greatly which was only 0.47% of that in the normal at 6 weeks. It remained low until 12 weeks after neurorrhaphy, which was 0.72% of the normal side. It increased obviously to 0.83 times of normal sides at 18 weeks and didn't changed there after. CONCLUSION: The state of reinnervation determines the quantity of neuromuscular junctional N-AchR.
OBJECTIVE: To determine the precise allelic loss on chromosome 3p14 and discuss the possible relations between loss of heterozygosity (LOH) and EBV infection, clinical stage and clinic-pathology of nasopharyngeal carcinoma (NPC). METHODS: Six high dense microsatellite marker on chromosome 3p14 were selected to examine LOH in 32 cases of NPC. RESULTS: 23 of 32 (71.9%) tumors were deleted for at least one locus of six loci. High frequencies of LOH (> 40%) were observed at loci D3S1300(50.0%), D3S1313(46.4%) and D3S1312(44.4%). 12 cases showed LOH in one contiguous and nonrandom region. The smallest common deletion region seems likely to lie between D3S1313 and D3S1312. Relations between LOH on 3p14 and clinical stage and EBV infection were observed. The frequency of LOH was 70.0% in 30 cases of poor-differentiated squamous cell carcinoma. 2 cases of vesicular nucleus cell carcinoma had LOH at two loci. CONCLUSION: The high deletion rate on 3p14 in NPC indicates that there might be a putative tumor suppressor gene related to the development and progression of NPC.
OBJECTIVE: To observe the characteristic immunodeficiency syndrome of the rapid fatal type of simian immunodeficiency virus (SIV) infected monkeys. METHODS: Eighty rhesus monkeys and 4 cynomolgus monkeys were intravenously inoculated with SIVmac or SIVmac251. The virus isolation and viral titer, estimation by indirect immunofluroresence and viral antibody were determined periodically from monkeys' plasma; lymph node biopsies were performed for pathohistological examination. RESULTS: Twelve out of 84 macaque (14.2%) died of rapid progressive type after inoculation of SIVmac and SIVmac251 in the duration 3 to 4 months. Dying monkeys showed persistent high viremia and low level titre antibody. Eight of 10 pathohistological changes showed severe depletion of lymphoid tissue in spleen and lymph nodes, there were remarkable immunodeficiency with opportunity infection. The other two monkeys appeared moderate lymphoid tissue deletion and hyperplasia without opportunity infections. The survived monkeys' (72/84) lymph nodes biopsies revealed hypoplasia of lymphoid tissue. CONCLUSIONS: The characteristic immunodeficiency syndrome of rapid fatal type of simian immunodeficiency virus infected monkeys could be made with persistent high viremia, low level antibody, severe lymphoid tissue deletion in lymph nodes and spleen, as well as complicated opportunity infections.
OBJECTIVE: To probe into the pathogenic mechanisms of paraneoplastic encephalomyelitis (PEM) or sensory neuronopathy(PSN). METHODS: The serum and cerebral spinal fluid(CSF) anti-Hu antibodies and titers in 16 patients with PEM and 14 patients with PSN were detected with indirect immunohistochemistry (ABC) method. Intrathecal IgG synthesis and antibody specific activity (ASA) were calculated with Schuller's formulas according to the titers of the anti-Hu antibodies in the serum and CSF of the patients. Anti-Hu antibodies were identified by detecting the antigens of the nuclear extracts from the human cerebral cortex neurons with Western blot analysis. IgG in the serum and CSF and the albumin in the CSF were tested with electroimmunodiffusion method. RESULTS: The serum and CSF anti-Hu antibody titers in patients with PEM were significantly higher than those in patients with PSN (P < 0.001). A ratio of intrathecal ASA/serum ASA of anti-Hu antibody > 2 in 14 (88%) of the 16 patients with PEM and one (7%) patient with PSN indicated that the patients with PEM had a positive intrathecal anti-Hu antibody synthesis (P < 0.001). The Rankin scores are 4.5 +/- 1.7 in patients with PEM and 3.0 +/- 1.4 in patients with PSN (P < 0.01). Patients with PEM were more disabled than those with PSN. CONCLUSIONS: The detection of intrathecal ASA/serum ASA ratio for identifying the anti-Hu antibody intrathecal synthesis is valuable in judging the severity of disease and prognosis in patients with paraneoplastic syndromes of nervous system.
The visible spectra of forty-five synthesized polyaluminium ferric chloride (PAFC) aqueous solutions with different [OH]/[Al + Fe] (B) and nAl/nFe(molar ratio) were investigated. The results showed that their absorbances A of shoulder at 460 nm are all linear interrelationship with their B. We made the curve of absorbance A of PAFC with same B vs. nAl/nFe, there was a turning point. All of these points just located at the places of pH value rising higher in pH- nAl/nFe diagrams. For these reason, we thought that these points stand for the dynamic equilibrium of OH- between the polynucleus hydroxyl Fe(III) and Al(III). These points made certain relationship among the absorbance A at 460 nm, basicities and total Fe(III) concentration of PAFC solutions.
The present study investigated the involvement of the transcription factor NF-kappaB in the expression of an anti-apoptotic gene, bcl-x, using a murine macrophage cell line and peritoneal macrophages from both wild type (p50(+/+)) and NF-kappaB p50 gene knockout (p50(-/-)) mice. Increased expression of Bcl-x protein was observed in native and silica-exposed p50(-/-) macrophages in which the NF-kappaB p65-containing complex was predominantly induced. Co-transfection experiment using a bcl-x promoter reporter construct and an expression vector for NF-kappaB p50 or p65 indicates that p65, but not p50, up-regulates the promoter activity of the bcl-x gene. DNA sequence analysis revealed that there are several kappaB-like sites within the 5'-flanking region of the bcl-x gene. Electrophoretic mobility shift assay suggested differences in binding of the NF-kappaB complexes to these putative NF-kappaB binding sites of the bcl-x gene.
STUDY DESIGN: The recording of electromyographic responses from the in vivo lumbar multifidus of the cat, obtained while cyclic loading was applied as in occupational bending/lifting motion over time. OBJECTIVES: To determine whether the effectiveness of stabilizing reflexive muscular activity diminishes during prolonged cyclic activity; the recovery of lost muscle activity by a 10-minute rest; and whether such diminished muscular activity is caused by fatigue, neurologic habituation, or desensitization of mechanoreceptors in spinal viscoelastic tissues resulting from its laxity. SUMMARY OF BACKGROUND DATA: The literature repeatedly confirms observation that cyclic occupational functions expose workers to a 10-fold increase in episodes of low back injury and pain. The biomechanical evidence indicates that creep in the viscoelastic tissues of the spine causes increased laxity in the intervertebral joints. The impact of cyclic activity on the function of the muscles, which are the major stabilizing structures of the spine, is not known. METHODS: Electromyography was performed from the L1 to L7 in vivo multifidus muscles of the cat, while cyclic passive loading of 0.25 Hz was applied to L4-L5. Cyclic loading was applied for 50 minutes, followed by 10 minutes rest and a second 50-minute cyclic loading session. A third 50-minute cyclic loading period also was applied after the preload was reset to 0.5 N to offset the effect of laxity. RESULTS: Reflexive muscular activity was recorded from the multifidus muscles of all lumbar levels at the initiation of the first 50 minutes of cyclic loading. Activity recorded on electromyography quickly diminished with each cycle during the first 8 minutes of loading to 15% of its initial value. A slower decrease in muscular activity was evident throughout the remaining period, settling at 5% to 10% of its initial level by the end of 50 minutes. A 10-minute rest provided a 20% to 25% recovery of the electromyographic activity, but that was lost within the first minute of cycling. Offsetting the laxity in the spine resulted in full restoration of the electromyographic activity at all lumbar levels. CONCLUSIONS: The creep induced in the viscoelastic tissues of the spine as a result of cyclic loading desensitizes the mechanoreceptors within, which is manifest in dramatically diminished muscular activity, allowing full exposure to instability and injury, even before fatigue of the musculature sets in.
STUDY DESIGN: Electromyographic responses from the lumbar multifidus muscle of the cat were recorded in vivo during 50 minutes of cyclic loading followed by 2 hours of rest. OBJECTIVE: To determine the rate of recovery of reflexive muscular stabilizing activity resulting from rest after viscoelastic laxity induced by 50 minutes of cyclic loading. SUMMARY OF BACKGROUND DATA: Muscular forces from agonists and antagonists were repeatedly shown to be the most significant stabilizing structures of the lumbar spine. Reflexive muscular coactivation force from the multifidus muscle elicited by mechanoreceptors in the spinal viscoelastic structures were, however, shown to diminish drastically with the onset of laxity in the viscoelastic structures. Data describing the rate of recovery of reflexive muscular coactivation forces resulting from rest after cyclic loading were not found. METHODS: Cyclic loading of the lumbar spine at 0.25 Hz was applied to L4-L5 for 50 minutes while electromyograms from the multifidus muscles of L1-L2 to L6-L7 were recorded. A rest period of up to 2 hours was given, during which electromyographic responses and load were measured every 10 minutes to sample recovery of laxity and reflexive muscular activity. RESULTS: Load and electromyographic response demonstrated an exponential decrease during the 50 minutes of cyclic loading. The first 10 minutes of rest allowed a significant recovery in laxity and muscle activity, with additional slow recovery over the next 20 to 30 minutes. The electromyographic response and load were increasing at an extremely slow rate thereafter. Overall, 2 hours of rest yielded only a 20% to 30% recovery in electromyographic response. Full recovery was never observed. A biexponential model was developed to predict loss and recovery of reflexive muscular activity and viscoelastic tension with laxity. CONCLUSIONS: Laxity in the viscoelastic structures of the lumbar spine desensitizes the mechanoreceptors within and causes loss of reflexive stabilizing forces from the multifidus muscles. The first 10 minutes of rest after cyclic loading results in fast partial recovery of muscular activity. However, full recovery is not possible even with rest periods twice as long as the loading period, placing the spine at an increased risk of instability, injury, and pain.
The PTEN/MMAC1/TEP (PTEN) tumor suppressor gene at 10q23.3 is mutated in multiple types of sporadic tumors including breast cancers and also in the germline of patients with the Cowden's breast cancer predisposition syndrome. The PTEN gene encodes a multifunctional phosphatase capable of dephosphorylating the same sites in membrane phosphatidylinositols phosphorylated by phosphatidylinositol 3'-kinase (PI3K). We demonstrate herein that loss of PTEN function in breast cancer cells results in an increase in basal levels of phosphorylation of multiple components of the P13K signaling cascade as well as an increase in duration of ligand-induced signaling through the P13K cascade. These alterations are reversed by wild-type but not phosphatase inactive PTEN. In the presence of high concentrations of serum, enforced expression of PTEN induces a predominant G1 arrest consistent with the capacity of PTEN to evoke increases in the expression of the p27Kip1 cyclin dependent kinase inhibitor. In the presence of low concentrations of serum, enforced PTEN expression results in a marked increase in cellular apoptosis, a finding which is consistent with the capacity of PTEN to alter the phosphorylation, and presumably function, of the AKT, BAD, p70S6 kinase and GSK3 alpha apoptosis regulators. Under anchorage-independent conditions, PTEN also induces anoikis, a form of apoptosis that occurs when cells are dissociated from the extracellular matrix, which is enhanced in conjunction with low serum culture conditions. Together, these data suggest that PTEN effects on the PI3K signaling cascade are influenced by the cell stimulatory context, and that depending on the exposure to growth factors and other exogenous stimuli such as integrin ligation, PTEN can induce cell cycle arrest, apoptosis or anoikis in breast cancer cells.
The mass of the central black holes in Seyfert galaxies and QSOs can be determined from the broad emission lines and the reverberation method. Using the measured black hole mass and the bolometric or ionizing luminosity, the accretion rate can be estimated. Compiling a sample of Seyfert 1 galaxies and QSOs with reliable central masses, estimated ionizing luminosities, and X-ray spectral slopes, we find that the X-ray spectral slope strongly correlates with the accretion rate. The objects in the sample are found to be distributed in two distinct classes in the spectral index versus log&parl0;Lion&solm0;LEdd&parr0;-plane. We argue that these two classes may correspond to advection-dominated accretion flow (ADAF) and thin disk accretion. The observations of a "two-state" Seyfert 1 galaxy, 1H 0419-577, confirm our results. Detailed fitting of the spectra of individual Seyfert 1 galaxies and QSOs using ADAF and/or thin disk models should further clarify the two-class classification.
Angiostatin protein, which comprises the first four kringle domains of plasminogen, is an endogenous inhibitor of angiogenesis that inhibits the growth of experimental primary and metastatic tumors. Truncation of Angiostatin K1-4 to K1-3 retained the activity of Angiostatin. We recombinantly expressed full-length human Angiostatin protein corresponding to the first four kringle domains of human plasminogen and a truncated form of the Angiostatin protein, kringles 1-3. Purified recombinant Angiostatin K1-3 and K1-4 proteins inhibited the formation of experimental B16-BL6 lung metastases by greater than 80% when administered at 30 nmol/kg/day. We demonstrate for the first time that Angiostatin protein, consisting of the first three kringle domains of human plasminogen, has in vivo biological activity in this assay indistinguishable from that of the full-length Angiostatin K1-4 protein and that the fourth kringle of plasminogen, when linked in sequence to K1-3, plays no direct role in the antitumor activity of Angiostatin.
The transcription factor activator protein-1 (AP-1) reportedly plays an important role in the induction of neoplastic transformation and multiple genes involved in cell proliferation, differentiation, and inflammation. To investigate the mechanisms of silica-induced carcinogenesis, AP-1-luciferase reporter transgenic mice were used as an in vivo model, whereas the JB6 mouse epidermal cell line and a rat lung epithelial cell line were employed as in vitro models to study the effects of silica at the molecular level. Freshly fractured silica caused an 8-fold increase in AP-1 activity in JB6 cells and a 2.5-fold increase in rat lung epithelial cells. The induction of AP-1 activity in cultured cell lines was time- and dose-dependent. Intratracheal administration of silica was also able to induce AP-1 transactivation in transgenic mice. AP-1 activation was first observed at 2 days after silica administration and reached its maximum at 3 days post-exposure of the mice to silica. The signal transduction pathways for AP-1 activation were also investigated using these cell lines. The results demonstrate that freshly fractured silica stimulates mitogen-activated protein kinase (MAPK) family members, as determined by the phosphorylation of p38 MAPK and extracellular signal-regulated protein kinases (ERKs). Inhibition of ERKs with PD98059 or of p38 with SB203580 significantly inhibited silica-induced AP-1 activation. These findings demonstrate for the first time that freshly fractured silica induces AP-1 activation, which may be mediated through p38 MAPK and ERK pathways. Unraveling the complex mechanisms associated with these events may provide insights into the initiation and progression of silica-induced carcinogenesis.