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Biomedical subjects

Bin Hu

Publications and source records attributed to Bin Hu.

At least 109 records · Page 6Linked to original sources
PubMed2003

[Amplification of RIT1 in hepatocellular carcinoma and its clinical significance].

BACKGROUND & OBJECTIVE: Previous study has demonstrated that high frequent gain of 1q was detected in hepatocellular carcinoma (HCC), 1q21-22 was identified as the minimum overlapping amplified region and might contain the candidate oncogenes involved in HCC. RIT1 gene is located in 1q21.3 region and is a member of Ras subfamily. RIT1 protein is similar to Ras protein in molecular structure and functions. It was speculated that RIT1 gene might be a candidate oncogene in HCC. So, the amplification of RIT1 gene was examined in HCC and was linked with the clinical indicators in this study to explore the possible functions of RIT1 gene in HCC development and progression. METHODS: The fluorescence quantitative polymerase chain reaction(FQ-PCR) method was established successfully. The number of RIT1 gene DNA copies was examined in the tumor tissues and its paratumor tissues from 43 patients with HCC by PE ABI 7000 Sequence Detector. The ratio of the number of RIT1 gene DNA copies between the tumor tissue and its paratumor tissue represented the extent of amplification of RIT1 gene DNA. RESULTS: RIT1 gene DNA was amplified in 11 cases (25.6%)among 43 patients. The mean survival time (15 months) of the RIT1 gene-amplification group is significantly shorter than that (34 months) of the non-amplification group (P = 0.0009); furthermore, the pathological grade and the extent of liver cirrhosis were significantly different between the RIT1 gene-amplification group and the non-amplification group (P< 0.01). CONCLUSION: The amplification of RIT1 gene might be one of the activation ways in HCC and might play an important role in HCC development and progression.

Adult↗
PubMed2003

[The effects of pH in artificial saliva on the corrosion resistance of magnetic retainers].

OBJECTIVE: The aim of this article was to discover the corrosion resistance of magnetic attachments, which were encapsulated in stainless steel, when pH value of artificial saliva was lower than normal. METHODS: Three kinds of magnetic retainers were exposed for 6 months to artificial saliva with pH ranging from 5.6 to 7.0, thermostated at 36.5 degrees C. This study included electrochemical test as polarization curves, chemical test as immersion test and SEM to analyze the corrosion behavior of the materials. RESULTS: Fe3+ ions in stainless steel released more than ten times in an environment pH 5.6 than pH 7.0. The higher concentration of H+, the more elemental release. That pH value of artificial saliva reduced may affect the corrosion speed. The magnetic retainers were not resistant to acidic environments during exposure. CONCLUSION: Transient exposure of stainless steel to an acidic oral environment can increase elemental release significantly. So acid resistance of magnetic retainers was relatively weak, and it would affect the life span of magnets.

Corrosion↗
PubMed2003

Effects of stanozolol on bone mineral density and bone biomechanical properties of osteoporotic rats.

OBJECTIVE: To evaluate the effects of stanozolol on the bone mineral density (BMD) and bone biomechanical properties of rats with glucocorticoid (GC)-induced osteoporosis (OP). METHODS: Twenty-eight male Sprague-Dawley rats of 3-month old were randomly divided into Group A (the basal control group), Group B (the age-matched control group), Group C (GC-induced OP group) and Group D (stanozolol-administrated group), 7 in each group. The rats in Group A were killed when experiment commenced, and those in Group B were given normal saline ig., while those in Groups C and D received the prednisone acetate (4.5 mg/kg, twice a week) alone and in combination with stanozolol (0.5 mg/kg, 6 times a week), respectively. Ninety days later, the bilateral femur and the 5th lumbar vertebra of the rats were isolated for BMD test using dual-energy X-ray absorptiometry scanner, and the torsion test, three-point bending test and compression test using electronic testing device. RESULTS: Compared with Group B, the mean BMD of the femur and the 5th lumbar vertebra in Group C decreased by 14.64% (P<0.01), the BMD of the bilateral distal femoral segment and the 5th lumbar vertebra decreased by 21.42% (P<0.01), 19.62% (P<0.05) and 23.48% (P<0.01) respectively. The load that the femur withstood in three-point bending test decreased by 17.1% (P<0.05), and the other biomechanical parameters also declined. When compared with Group C, the BMD in Group D increased, the torsional angle of the femur increased by 72.5% (P<0.05) and the other biomechanical parameters also tended to increase. CONCLUSIONS: BMD and biomechanical properties of the rat femur and the 5th lumbar vertebra decrease in response to a long-term GC administration, which can be prevented by stanozolol.

Animals↗
PubMed2003

[Kidney-targeting characteristics of N-acetyl-L-glutamic prednisolone prodrug].

AIM: To study the in vivo distribution of N-acetyl-L-glutamic prednisolone (ACEP) and to investigate the renal targeting characteristics of the prodrug. METHODS: The concentrations of prednisolone in organs at predetermined time were assayed by HPLC after intravenous administration of ACEP or prednisolone to Kunming mice. The adverse effects were evaluated by testing the bone mineral densities (BMD) of Wistar rats. RESULTS: The concentrations of prednisolone in kidney 15 min after i.v. administration were (86 +/- 8) microgram.g-1 for ACEP group, (57 +/- 4) microgram.g-1 for prednisolone group; 60 min after i.v. administration were (67 +/- 5) microgram.g-1 for ACEP group, (42 +/- 4) microgram.g-1 for prednisolone group. BMDs were (0.08 +/- 0.03) g.cm-2 and (0.14 +/- 0.06) g.cm-2 for prednisolone and ACEP-treated Wistar rats respectively. CONCLUSION: Compared with the parent drug prednisolone, ACEP has kidney-targeting behavior and lower toxicity (n = 5, P < 0.001).

Absorptiometry, Photon↗
PubMed2003

[The effect on anti-acid corrosion resistance of Ni-Cr alloy coating titanium].

OBJECTIVE: The aim of this study was to investigate the variation of the corrosion resistance of Ni-Cr alloy in acid environment before and after coating titanium in vitro. METHODS: 1. Surface treatment using sol-gel technique of coating titanium. The steps were as follows: (1) Pre-treatment: sanding, washing and activation in order to remove the oxidative product; (2) The preparation of sol: some small charged particles produced by the hydrolytic reaction, and formed sol. These particles would congeal into extremely small ones (diameter usually is 5 microns); (3) Coating; (4) Heat treatment: The organism was resolved and volatilizeed at high temperature, and the atoms of Ti were left. These atoms of Ti were very active and could combine firmly with the atoms on the surface awaiting of treatment. 2. CONDITIONS: artificial saliva; pH = 7.0 and pH = 5.6; temperature: 36.5 degrees C 3. Electrochemical test: polarization curve; instrument: ZF-3 poteniostat. RESULTS: Before coating titanium, when pH was 7.0, the electrode potential of Ni-Cr alloy was -160 mV, and the self-corrosion current density was 0.262 microA cm-2; when pH = 5.6, the data were -182 mV and 0.352 microA cm-2, respectively. This result showed that when pH value reduced, the potential and current density descended, too. This indicated that the material was easy to be corroded. After coating titanium, when pH value was 7.0, the potential was -71 mV, the self-corrosion current density was 0.152 microA cm-2; when pH = 5.6, the data were -89 mV and 0.174 microA cm-2. This indicated that the corrosion rate of material descended evidently after coating titanium in acid environment. CONCLUSION: (1) Not only before coating Ti but also after coating, the corrosion resistance of Ni-Cr alloy would descend in acid environment;(2) In acid environment, the corrosion resistance of Ni-Cr alloy after coating titanium was superior to that of the material before coating. So was in neutral environment.

Chromium↗
PubMed2003

[Diagnosis and treatment for pulmonary thromboembolism in postthoracotomy patients].

OBJECTIVE: To report the experience in the diagnosis and treatment of pulmonary thromboembolism (PTE) in postthoracotomy patients and to analyze current problems in this field. METHODS: From January 2001 to June 2002 we diagnosed and treated 5 patient who had pulmonary thromboembolism, 72-168 hours after thoracotomy (male 4, female 1, mean age 63 years). Symptoms include breathholding, chest pain, palpitation, coma and so on. Physical signs include tachypnea, hypotension and tachycardia. We utilized spiral CT pulmonary artery angiography (SCTPA) and Doppler echocardiography to judge PTE. Pulmonary artery interventional therapy was used in 3 cases and total body thrombolysis in 1. RESULTS: 4 patients recovered with no complication and recurrence; 1 patient died from congestive heart failure and respiratory failure. CONCLUSION: Deep venous thrombosis (DVT) and PTE are related to the surgical intervention, chest tumor and thoracotomy is high risk factors. Screenage examination is primary to used. Pulmonary artery interventional therapy is safe to the postthoracotomy patients. Preventive measures is very important in the high-risk group.

Aged↗
PubMed2002

Heme activates the heme oxygenase-1 gene in renal epithelial cells by stabilizing Nrf2.

The mechanism of heme oxygenase-1 gene (ho-1) activation by heme in immortalized rat proximal tubular epithelial cells was examined. Analysis of the ho-1 promoter identified the heme-responsive sequences as the stress-response element (StRE), multiple copies of which are present in two enhancer regions, E1 and E2. Electrophoretic mobility shift assays identified Nrf2, MafG, ATF3, and Jun and Fos family members as StRE-binding proteins; binding of Nrf2, MafG, and ATF3 was increased in response to heme. Dominant-negative mutants of Nrf2 and Maf, but not of c-Fos and c-Jun, inhibited basal and heme-induced expression of an E1-controlled luciferase gene. Heme did not affect the transcription activity of Nrf2, dimerization between Nrf2 and MafG, or the level of MafG, but did stimulate expression of Nrf2. Heme did not influence the level of Nrf2 mRNA but increased the half-life of Nrf2 protein from approximately 10 min to nearly 110 min. These results indicate that heme promotes stabilization of Nrf2, leading to accumulation of Nrf2. MafG dimers that bind to StREs to activate the ho-1 gene.

Animals↗
PubMed2002

Multiple basic-leucine zipper proteins regulate induction of the mouse heme oxygenase-1 gene by arsenite.

The mechanism of heme oxygenase-1 (ho-1) gene activation by arsenite was examined. Arsenite-stimulated expression of a ho-1 promoter/luciferase chimera in a dose-dependent manner in mouse hepatoma (Hepa) cells. Mutation analyses identified the arsenite-responsive sequence as the stress-response element (StRE), which resembles the binding sites for the AP-1 superfamily of basic-leucine zipper factors. In electrophoretic mobility shift assays, up to seven specific StRE-protein complexes were routinely detected using extracts from untreated Hepa cells whereas a single complex was typically observed after treatment with arsenite. Antibody "supershift" experiments identified Nrf2, JunD, and ATF3 in control complexes and the amount of these factors increased significantly in the arsenite-induced complex. MafG, ATF2, FosB, and JunB were also detected in the arsenite complex. Activation of a StRE-dependent luciferase gene by arsenite was inhibited to varying degrees by dominant-negative mutants of Nrf2, MafK, c-Fos, and CREB but most strongly with the latter. Together, these results implicate multiple basic-leucine zipper transcription factors in ho-1 gene activation by arsenite.

Activating Transcription Factor 2↗
PubMed2002

A structural mechanism of integrin alpha(IIb)beta(3) "inside-out" activation as regulated by its cytoplasmic face.

Activation of the ligand binding function of integrin heterodimers requires transmission of an "inside-out" signal from their small intracellular segments to their large extracellular domains. The structure of the cytoplasmic domain of a prototypic integrin alpha(IIb)beta(3) has been solved by NMR and reveals multiple hydrophobic and electrostatic contacts within the membrane-proximal helices of its alpha and the beta cytoplasmic tails. The interface interactions are disrupted by point mutations or the cytoskeletal protein talin that are known to activate the receptor. These results provide a structural mechanism by which a handshake between the alpha and the beta cytoplasmic tails restrains the integrin in a resting state and unclasping of this interaction triggers the inside-out conformational signal that leads to receptor activation.

Amino Acid Sequence↗
PubMed2002

Activation of protein kinase C beta II by the stereo-specific phosphatidylserine receptor is required for phagocytosis of apoptotic thymocytes by resident murine tissue macrophages.

We showed previously that protein kinase C (PKC) is required for phagocytosis of apoptotic leukocytes by murine alveolar (AMø) and peritoneal macrophages (PMø) and that such phagocytosis is markedly lower in AMø compared with PMø. In this study, we examined the roles of individual PKC isoforms in phagocytosis of apoptotic thymocytes by these two Mø populations. By immunoblotting, AMø expressed equivalent PKC eta but lower amounts of other isoforms (alpha, betaI, betaII, delta, epsilon, mu, and zeta), with the greatest difference in betaII expression. A requirement for PKC betaII for phagocytosis was demonstrated collectively by phorbol 12-myristate 13-acetate-induced depletion of PKC betaII, by dose-response to PKC inhibitor Ro-32-0432, and by use of PKC betaII myristoylated peptide as a blocker. Exposure of PMø to phosphatidylserine (PS) liposomes specifically induced translocation of PKC betaII and other isoforms to membranes and cytoskeleton. Both AMø and PMø expressed functional PS receptor, blockade of which inhibited PKC betaII translocation. Our results indicate that murine tissue Mø require PKC betaII for phagocytosis of apoptotic cells, which differs from the PKC isoform requirement previously described in Mø phagocytosis of other particles, and imply that a crucial action of the PS receptor in this process is PKC betaII activation.

Acetophenones↗
PubMed2002

Synthesis and characterization of novel ceramide analogs for induction of apoptosis in human cancer cells.

A variety of anti-cancer drugs elevate endogenous ceramide, thereby inducing apoptosis in tumor cells. Recently, we have introduced novel ceramide analogs of the beta-hydroxy alkyl amide type, which trigger pro-apoptotic signaling pathways without prior elevation of endogenous ceramide. They induce apoptosis specifically in rapidly dividing neuroblastoma cells, but not in resting or differentiated cells. We characterize new ceramide mimics that have been derived from N-acylation of serinol (S), diethanolamine (B), propanolamine (P), and tris(hydroxy-methyl)methylamine (T) with myristic (14), palmitic (16), or oleic (18) acid. The water solubility of these compounds exceeds that of ceramide by more than 100-fold (up to 5 mM). Apoptosis of human neuroblastoma, glioma, medulloblastoma, and adenocarcinoma cells is induced by N-(2-hydroxy-1-(hydroxymethyl)ethyl)-palmitoylamide, C16-serinol (S16), N-(2-hydroxy-1-(hydroxymethyl)ethyl)-oleoylamide, C18-serinol (S18), N-bis(2-hydroxyethyl)-myristoyl-amide (B16), and N-tris(hydroxymethyl)methyl-oleoylamide (T18) within 60 min of incubation, and is completed even after removal of the compound from the medium. This is most likely due to a rapid uptake of the analogs followed by their slow release from the cells. Alteration of the acyl chain length to less than 14 methylene units, removal of the amino group, or reducing the number of hydroxyalkyl residues to less than two significantly lowers or eliminates the pro-apoptotic potential of these compounds. The target specificity of novel ceramide analogs for tumor cells, their water solubility, and fast pro-apoptotic mechanism indicates a high therapeutic potential for cancer treatment.

Apoptosis↗
PubMed2002

Activation of the mouse heme oxygenase-1 gene by 15-deoxy-Delta(12,14)-prostaglandin J(2) is mediated by the stress response elements and transcription factor Nrf2.

The mechanism of heme oxygenase-1 (ho-1) gene activation by 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) was examined. 15d-PGJ(2) stimulated expression of HO-1 mRNA and protein and of a mouse ho-1 gene promoter/luciferase fusion construct (HO15luc) in a dose-dependent manner in mouse hepatoma (Hepa) cells. HO15luc expression was not effected by troglitazone, a peroxisome proliferator-activated receptor-gamma (PPAR-gamma) ligand, but induction by 15d-PGJ(2) was abrogated by the antioxidant N-acetylcysteine. The primary 15d-PGJ(2) responsive sequences were localized to a 5' distal enhancer (E1) and identified as the stress-response element, previously shown to mediate ho-1 activation by several agents, including heme and heavy metals. Treatment of Hepa cells with 15d-PGJ(2) stimulated stress-response element-binding activity as judged by electrophoretic mobility shift assays. Antibody "supershift" experiments identified NF-E2 related factor 2 (Nrf2), but not Fos, Jun, or activating transcription factor/cyclic AMP response element binding protein transcription factors, within the 15d-PGJ(2)-induced complexes. Similarly, a dominant-negative mutant of Nrf2, but not of c-Jun or c-Fos, abrogated 15d-PGJ(2)-stimulated E1 transcription activity. Finally, prior induction of HO-1 in RAW264.7 mouse macrophages by 15d-PGJ(2) attenuated cell death caused by diesel exhaust particle extracts. These results demonstrate that induction of mouse HO-1 expression by 15d-PGJ(2) is independent of PPAR-gamma but dependent on oxidative stress, is regulated by the oxidative stress-activated transcription factor Nrf2, and provides cytoprotective activity.

Animals↗
PubMed2002

Differential distribution of burst and single-spike responses in auditory thalamus.

The medial geniculate body (MGB) of the auditory thalamus comprises lemniscal and nonlemniscal neurons that project to the primary auditory cortex and limbic structures, respectively. Here we show that in anesthetized guinea pigs, MGB responses to a noise-burst stimulus exhibit distinct and synaptic pathway-specific firing patterns. The majority of nonlemniscal MGB cells exhibited bursting responses, whereas lemniscal neurons discharged mainly single or spike doublets. The burst firing is delayed in nonlemniscal neurons and exhibited several features that are characteristics of those mediated by low-threshold Ca(2+) spikes. Such a synaptic pathway-specific allocation of bursting and single-spike firing patterns is consistent with the notion of parallel processing of auditory information in thalamocortical system.

Acoustic Stimulation↗
PubMed2002

Recognition and phagocytosis of apoptotic T cells by resident murine tissue macrophages require multiple signal transduction events.

Macrophages (Mø) ingest apoptotic cells with unique effects on their cytokine production, but the signaling pathways involved are virtually unknown. Signal transduction in response to recognition of apoptotic thymocytes by resident murine alveolar (AMø) or peritoneal (PMø) Mø was studied by in vitro phagocytosis assay. Phagocytosis was decreased in a dose-dependent and nontoxic manner by inhibiting phosphatidylinositol 3 kinase (wortmannin and LY294002), protein tyrosine phosphorylation (herbimycin A, genistein, piceatannol, and for AMø only, PP2), and protein kinase C (staurosporine, Gö 6976, and calphostin C). Exposure of Mø to apoptotic or heat-killed thymocytes, but not to viable thymocytes, activated ERK1/2 rapidly, as detected by specific phosphorylation, but did not activate NF-kappaB or MAP kinases p38 or JNK. Mø phagocytosis of apoptotic T cells requires tyrosine, serine/threonine, and lipid phosphorylation. Mø recognition of apoptotic T cells triggers rapid but limited MAP kinase activation.

Animals↗
PubMed2002

[The application of inductively coupled plasma atomic emission spectrometry/mass spectrometry in the trace elements and speciation analysis of traditional Chinese Medicine].

A review on the content and speciation analysis of trace element in traditional chinese medicine (TCM) by ICP-AES/MS was presented. The study is mainly focused on the following subjects: sample digestion techniques; determination and speciation analysis of trace elements. The development trend of this area in the near future is briefly introduced. 58 references are cited. The results show that the microwave digestion techniques is a idea pretreatment method of sample for tradition chinese medicine; ICP-AES/MS and all kinds of hyphenated techniques for atomic optical/mass spectrometry/chromatography are very useful for the determination and speciation analysis of trace elements in TCM.

Drug Contamination↗
PubMed2002

[Bone mineral density and biomechanical effects of Chinese herbal drug Yanhuogubao on experimental osteoporosis in rats].

OBJECTIVE: To explore bone mineral density and biomechanical effects of Chinese herbal drug Yanhuogubao on steroid hormone-induced osteoporosis in rats. METHODS: Male, 3-month-old Sprague-Dawley rats were randomly divided into 4 groups (n = 7), the basal group, the age control group, the hormone group (4.5 mg/kg prednisone acetate, twice a week) and Yanhuogubao (1.5 g/kg/d) group. The bone mineral densities and the mechanical characters measurements of femurs and 5th lumbar vertebrae in every group were made by using DEXA and SWD-10 electronic universal material testing machine. RESULTS: The bone mineral densities on femora and 5th lumbar vertebrae in hormone group decreased, and the loads imposed on the femoral trunk in three-point bending test decreased by 17.1% (P < 0.05), though the rest parameters tended to decrease in comparison with control group. In the meantime, Yanhuogubao can prevent prednisone acetate-induced the bone mineral densities and mechanical characters of femurs and lumbar vertebrae in rats from decline, compared with hormone group. CONCLUSION: When steroid hormone was used for a long time, the bone mineral densities and mechanical characters of femora and 5th lumbar vertebrae in the rats would be led to decrease, on the contrary, Yanhuogubao could arrest the decline of bone mineral densities and mechanical characters of rat skeleton.

Animals↗
PubMed1990

Electrophysiology and Pharmacology of the Corticothalamic Input to Lateral Thalamic Nuclei: an Intracellular Study in the Cat.

Though most experimental evidence indicates that the corticothalamic (CT) pathway would exert a direct excitatory action on thalamic relay neurons, the electrophysiological features of this excitation have never been clearly described. A methodological problem in previous electrophysiological studies was that direct corticofugal effects on relay cells could not be separated from those mediated by collateral activation of reticular thalamic neurons. In the present study, the reticular complex was lesioned by kainic acid and the CT response of relay neurons of the ventral lateral nucleus was recorded intracellularly in cats under pentobarbital or urethane anaesthesia. Following reticular thalamic lesions, a prominent depolarization was triggered in thalamic relay cells by stimulation of the CT pathway. This depolarization strongly drove spike discharges, and its amplitude augmented when the stimulation rate exceeded 2 Hz. Tetanizing the CT input with short trains (100 - 200 Hz for 200 - 300 ms) produced a similar augmentation to test volleys for 15 - 30 s after the tetanos. The CT excitation and its frequency-dependent augmentation were depressed by ketamine injection or by local application of N-methyl-D-aspartate (NMDA) antagonists. The augmenting phenomenon appeared strictly homosynaptic. For instance, it did not appear during repetitive stimulation of the cerebellar input, nor did the CT input potentiate subthreshold synaptic potentials of cerebellar origin during a conditioning procedure. Conversely, the cerebellar excitation was depressed when it occurred during the CT depolarization. It is concluded that the direct synaptic responses induced by CT fibres in relay neurons are mediated at least partly by the activation of NMDA receptors. Moreover, the marked non-linear additivity of cerebellar and CT synaptic potentials raises questions concerning the presumed improvement of thalamic transmission of peripheral informations ensured by the CT input. Instead, both inputs could compete for control of the firing of thalamic neurons. The numerical importance of CT fibres and the strong augmenting mechanism operating at synaptic sites in the thalamus suggest that the role of the thalamus is not only to transfer peripheral informations toward the cortex, but also and mainly to feed back to the cortex a modified copy of its own neuronal constructs.

Journal Article↗