Biomedical subjects

Feng Bao

Publications and source records attributed to Feng Bao.

At least 19 recordsLinked to original sources

PubMed2006

MnS hierarchical hollow spheres with novel shell structure.

High yields of MnS microspheres with novel hierarchical structure were prepared through a simple solution method. Field emission scanning electron microscopy and transmission electron microscopy analyses reveal that the microsphere has a core-shell structure: the interior hollow sphere is covered by a shell consisting of nanorod arrays. Interestingly, the nanorod is a wurtzite (WZ)/zinc blende (ZB) phase admixture with a large amount of stacking faults/twins. The alternation of WZ and ZB along the growth direction of the nanorod enables it to exhibit the features of a quantum well. Furthermore, the WZ/ZB admixture structure could also be regarded as a type II homomaterial heterostructure. All these features imply that the novel core-shell structure has great potential for applications, among them the quantum well photoelectrical and heterostructure photoconduction fields.

Journal Article↗

PubMed2006

Effects of a novel tripeptide on neurological outcomes after spinal cord injury.

A biologically active tripeptide [phenylalanine glutamate glycine (feG)] derived from the submandibular gland has anti-inflammatory actions. We have shown that intravenous treatment with feG after spinal cord injury decreases the intraspinal infiltration of leukocytes and associated oxidative damage within 72 h after injury. The present study assessed effects of this treatment on chronic neurological outcomes after clip-compression spinal cord injury at the 12th thoracic segment. Locomotor scores of feG-treated rats were significantly higher than those of controls at 7 weeks after spinal cord injury. Treated rats had significantly less hind paw mechanical allodynia than controls at this time. In conclusion, the anti-inflammatory and anti-oxidative actions of feG treatment correlate with improved neurological outcomes after spinal cord injury.

Animals↗

PubMed2006

Shape control of monodisperse CdS nanocrystals: hexagon and pyramid.

The wurtzite CdS nanocrystals with hexagonal or pyramidal geometries were selectively synthesized by tuning the molar ratio of Cd and S precursors in the solution system. For hexagonal nanocrystals, a 2-D or 3-D superlattice assembly could be obtained due to the narrow particle size distribution. The pyramidal CdS nanocrystals were divided into two geometries: the hexagon-based pyramid and the triangle-based pyramid. The realization of the pyramidal geometries further extends the shape multiformity of wurtzite CdS nanocrystals, which may bring new opportunities for the development of CdS semiconductors. The room-temperature absorption spectra of CdS nanoparticles with hexagonal and pyramidal morphologies exhibited a discrepancy in peak positions, revealing the existence of a profound shape-property relationship for the CdS nanophase.

Journal Article↗

PubMed2006

Metastable gamma-MnS hierarchical architectures: synthesis, characterization, and growth mechanism.

Preparation of shape-controlled metastable gamma-MnS semiconductor nanocrystals has been achieved on a large scale through a simple solvothermal method in the presence of PVP. The key strategy is the use of sulfur powder as sulfur source in ethylene glycol (EG) solvent that also acted as a weak reducing agent. Reaction parameters such as reaction time and temperature are found to be important in controlling various hierarchical architectures, such as homogeneous semi-hollow core-shell, hollow nanospheres, and nanowires. Transmission electron microscopy observations indicate that these hierarchical architectures are formed mainly via Ostwald ripening. The optical absorption measurements reveal that these novel architectures exhibit remarkable shift of absorption peak during the course of structural compaction and grain growth.

Journal Article↗

PubMed2006

Quasicubic alpha-Fe2O3 nanoparticles with excellent catalytic performance.

Uniform quasicubic alpha-Fe(2)O(3) nanoparticles enclosed by six identical {110} planes were synthesized by a simple solvothermal method. TEM investigations revealed that they were formed through oriented attachment of primary nanocrystals assisted by Ostwald ripening, and PVP surfactant played an important role in control over the final morphology of the products. These quasicubic nanoparticles could catalyze oxidation of almost 100% CO at a temperature of 230 degrees C, much lower than those of nanophases with flowerlike, hollow, or other forms of irregular external morphologies having various crystal planes exposed to the gas, indicating that the external morphology and especially the exposure crystal planes of alpha-Fe(2)O(3) nanocatalyst affect the catalytic activity more significantly than the traditionally accepted factors (such as high BET surface area, hollow structure, etc.) do for CO catalytic oxidation.

Journal Article↗

PubMed2006

Mn (III) tetrakis (4-benzoic acid) porphyrin administered into the intrathecal space reduces oxidative damage and neuron death after spinal cord injury: a comparison with methylprednisolone.

The metalloporphyrin Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP) is a cell-permeable superoxide dismutase mimetic and a broad-spectrum scavenger of reactive species. Since MnTBAP may not cross the blood-brain barrier, this study evaluated the therapeutic potential of MnTBAP to treat spinal cord injury (SCI; 25 g x cm) by directly administering it into the intrathecal space of the rat spinal cord. The cells in spinal sections removed at 24 h post-SCI were immunohistochemically stained with anti-4-hydroxynonenal (HNE), a marker of membrane lipid peroxidation (MLP); anti-nitrotyrosine (Ntyr), a marker of protein nitration; and anti-neuron-specific enolase (NSE) antibodies. Immunostained neurons were counted for quantitative evaluation. Pre-treatment 30 min before SCI with 1 mg/kg MnTBAP or 4-h post-SCI treatment with 2.5 mg/kg MnTBAP administered into the intrathecal space significantly reduced MLP and protein nitration, and increased the number of surviving neurons compared to vehicle controls. However, post-SCI treatment with a standard regimen of methylprednisolone sodium succinate (MPSS; 30 mg/kg followed by 5.4 mg/kg for maintenance, iv administration), the only drug used for clinical treatment of SCI, not only did not reduce MLP and neuron loss, it increased protein nitration compared with vehicle controls (two-way analysis of variance [ANOVA] followed by the Tukey test). These results demonstrate that pre- and post-intrathecal treatments with the low doses of MnTBAP provide sustained neuroprotection by preventing oxidative stress and that post-treatment with MnTBAP is superior to post-treatment with MPSS in preventing oxidative stress and resulting neuron loss.

Animals↗

PubMed2006

A therapeutic time window for anti-CD 11d monoclonal antibody treatment yielding reduced secondary tissue damage and enhanced behavioral recovery following severe spinal cord injury.

OBJECT: The purpose of this study was to investigate the therapeutic time window for antiinflammatory treatment within the first 24 hours of spinal cord injury (SCI). The authors have shown that an anti-CD11d antibody treatment attenuates leukocyte infiltration and improves neurological function when administered beginning 2 hours after SCI. A more clinically relevant time for the initiation of treatment after SCI, however, is 6 or more hours postinjury. METHODS: In Study 1, the T-4 vertebrae in four groups of rats were injured by a 50-g clip-induced compression method, and the anti-CD11d antibody (1 mg/kg) was intravenously administered starting 2, 6, 12, or 24 hours postinjury. All groups received subsequent doses at 24 and 48 hours, and animals were killed at 72 hours. The anti-CD11d antibody treatment starting at 6 hours postinjury caused significant attenuation of leukocyte infiltration, reactive oxygen species-associated enzymes, and secondary tissue damage. Based on these findings, Study 2 included two groups of rats receiving the aforementioned injury and treatment beginning at 6 hours postinjury (with subsequent treatments at 24 and 48 hours) with the anti-CD11d or a control antibody (1B7); these rats were then observed for 5 weeks. Basso-Beattie-Bresnahan (BBB) scores were significantly higher in anti-CD11d-treated rats (mean BBB score 8.9 +/- 0.1) than controls (mean BBB score 7.7 +/- 0.1) 5 weeks postinjury. Increases in mean arterial pressure during colon distension were smaller in anti-CD11d-treated rats (19.5 +/- 3.7 mm Hg) than in controls (37.4 +/- 4.7 mm Hg). CONCLUSIONS: These findings suggest that antiinflammatory treatments that reduce secondary tissue damage after SCI may be delayed until 6 hours postinjury and still be effective.

Animals↗

PubMed2005

Anti-CD11d antibody treatment reduces free radical formation and cell death in the injured spinal cord of rats.

Treatment with a monoclonal antibody (mAb) against the CD11d subunit of the leukocyte integrin CD11d/CD18 after spinal cord injury (SCI) decreases intraspinal inflammation and oxidative damage, improving neurological function in rats. In this study we tested whether the anti-CD11d mAb treatment reduces intraspinal free radical formation and cell death after SCI. Using clip-compression SCI in rats, reactive oxygen species (ROS) generated in injured spinal cord were detected using 2',7'-dichlorofluorescin-diacetate and hydroethidine as fluorescent probes. ROS in the injured cord increased significantly after SCI; anti-CD11d mAb treatment significantly reduced this ROS formation. Immunohistochemistry and western blotting were employed to assess the effects of anti-CD11d mAb treatment on spinal cord expression of gp91Phox (a subunit of NADPH oxidase producing superoxide) on formation of 4-hydroxynonenal (HNE, indicating lipid peroxidation) and on expression of caspase-3. We also assessed effects on cell death, determined by cell morphology. The expression of gp91Phox, formation of HNE, and cell death increased after SCI. Anti-CD11d mAb treatment clearly attenuated these responses. In conclusion, anti-CD11d mAb treatment significantly reduces intraspinal free radical formation caused by infiltrating leukocytes after SCI, thereby reducing secondary cell death. These effects likely underlie tissue preservation and improved neurological function that result from the mAb treatment.

Aldehydes↗

PubMed2005

Evolution of single crystalline dendrites from nanoparticles through oriented attachment.

Single crystalline PbMoO4 dendrites were prepared by a simple hydrothermal method in the presence of surfactants. The formation and evolution of these dendrites was investigated by transmission electron microscopy, and the results clearly showed that the dendritic structure was achieved through oriented attachment of nanoparticles along crystallographically specific direction while the traditional Ostwald ripening mechanism also acted to form the initial particles before attachment and smooth the morphology of the dendrites after attachment.

Journal Article↗

PubMed2005

Peroxynitrite generated at the level produced by spinal cord injury induces peroxidation of membrane phospholipids in normal rat cord: reduction by a metalloporphyrin.

The goal of the present study was to determine in vivo whether peroxynitrite, at the concentration and duration produced by SCI, contributes to membrane lipid peroxidation (MLP) after traumatic spinal cord injury (SCI) and the capability of a broad spectrum scavenger of reactive species, Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), to reduce MLP. This was accomplished by administering a peroxynitrite donor 3-morpholinosydnonimine (SIN-1) into the gray matter of an uninjured rat spinal cord through a microdialysis fiber to generate ONOO at the SCI-elevated levels. The resulting MLP was characterized by measuring the productions of extracellular malondialdehyde and of intracellular 4-hydroxynonenal. We demonstrated that extracellular SIN- 1 administration significantly increased the concentration of malondialdehyde (p < 0.001) and the numbers of hydroxynonenal-positive cells (p < 0.001) as compared to a control group in which ACSF was administered. Simultaneous administration of MnTBAP through a second microdialysis fiber significantly reduced SIN-1-induced malondialdehyde production (p < 0.001) and the numbers of HNE-positive cells (p < 0.001). There was no significant difference between MnTBAP-treated and ACSF-controls (p = 0.3). These results demonstrate in vivo that (1) SCI-produced levels of peroxynitrite sufficient to cause MLP, and therefore that peroxynitrite is an agent of secondary damage after acute SCI; (2) MnTBAP can efficiently reduce SIN-1-induced MLP.

Aldehydes↗

PubMed2005

Tailored reversible watermarking schemes for authentication of electronic clinical atlas.

It is accepted that digital watermarking is quite relevant in medical imaging. However, due to the special nature of clinical practice, it is often required that watermarking not introduce irreversible distortions to medical images. The electronic clinical atlas has such a need of "lossless" watermarking. We present two tailored reversible watermarking schemes for the clinical atlas by exploiting its inherent characteristics. We have implemented the schemes and our experimental results look very promising.

Algorithms↗

PubMed2004

Early anti-inflammatory treatment reduces lipid peroxidation and protein nitration after spinal cord injury in rats.

We investigated mechanisms by which a monoclonal antibody (mAb) against the CD11d subunit of the leukocyte integrin CD11d/CD18 improves neurological recovery after spinal cord injury (SCI) in the rat. The effects of an anti-CD11d mAb treatment were assessed on ED-1 expression (estimating macrophage infiltration), myeloperoxidase activity (MPO, approximating neutrophil infiltration), lipid peroxidation, inducible nitric oxide synthase (iNOS) and nitrotyrosine (indicating protein nitration) expression in the spinal cord lesion after severe clip-compression injury. Protein expression was evaluated by western blotting and immunocytochemistry. Lipid peroxidation was assessed by thiobarbituric acid reactive substances (TBARS) production. After anti-CD11d mAb treatment, decreased ED-1 expression at 6-72 h after SCI indicated reduced macrophage infiltration. MPO activity (units/g tissue) was reduced significantly from 114 +/- 11 to 75 +/- 8 (- 34%) at 6 h and from 38 +/- 2 to 22 +/- 4 (- 42%) at 72 h. After SCI, anti-CD11d mAb treatment significantly reduced TBARS from 501 +/- 61 to 296 +/- 17 nm (- 41%) at 6 h and to approximately uninjured values (87 nm) at 72 h. The mAb treatment also attenuated the expression of iNOS and formation of nitrotyrosine at 6-72 h after SCI. These data indicate that anti-CD11d mAb treatment blocks intraspinal neutrophil and macrophage infiltration, reducing the intraspinal concentrations of reactive oxygen and nitrogen species. These effects likely underlie improved tissue preservation and neurological function resulting from the mAb treatment.

Animals↗

PubMed2004

A smart-card-enabled privacy preserving E-prescription system.

Within the overall context of protection of health care information, privacy of prescription data needs special treatment. First, the involvement of diverse parties, especially nonmedical parties in the process of drug prescription complicates the protection of prescription data. Second, both patients and doctors have privacy stakes in prescription, and their privacy should be equally protected. Third, the following facts determine that prescription should not be processed in a truly anonymous manner: certain involved parties conduct useful research on the basis of aggregation of prescription data that are linkable with respect to either the patients or the doctors; prescription data has to be identifiable in some extreme circumstances, e.g., under the court order for inspection and assign liability. In this paper, we propose an e-prescription system to address issues pertaining to the privacy protection in the process of drug prescription. In our system, patients' smart cards play an important role. For one thing, the smart cards are implemented to be portable repositories carrying up-to-date personal medical records and insurance information, providing doctors instant data access crucial to the process of diagnosis and prescription. For the other, with the secret signing key being stored inside, the smart card enables the patient to sign electronically the prescription pad, declaring his acceptance of the prescription. To make the system more realistic, we identify the needs for a patient to delegate his signing capability to other people so as to protect the privacy of information housed on his card. A strong proxy signature scheme achieving technologically mutual agreements on the delegation is proposed to implement the delegation functionality.

Algorithms↗

PubMed2004

An anti-CD11d integrin antibody reduces cyclooxygenase-2 expression and protein and DNA oxidation after spinal cord injury in rats.

Our studies have shown that treatment with a monoclonal antibody (mAb) against the CD11d subunit of the leukocyte integrin CD11d/CD18 after spinal cord injury (SCI) decreases intraspinal inflammation, myeloperoxidase activity, lipid peroxidation and protein nitration, improving neurological function in rats. Using severe clip compression SCI in the rat, immunohistochemistry and western blotting were employed to assess the effects of an anti-CD11d mAb treatment on spinal cord cyclooxygenase-2 (COX-2) expression, formation of 8-hydroxy-2-deoxyguanosine (8-OHdG, a marker of RNA and DNA oxidation) and protein carbonylation (a marker of protein oxidation). We also assessed treatment effects on the expression of apurinic/apyrimidinic endonuclease (redox effector factor-1, APE/Ref-1), a multifunctional enzyme involved in the base excision repair of apurinic/apyrimidinic sites in DNA. The expression of COX-2 and formation of 8-OHdG and protein carbonyl groups were increased after SCI while APE/Ref-1 expression was decreased. Anti-CD11d mAb treatment clearly attenuated COX-2 expression and 8-OHdG and protein carbonyl formation and rescued APE/Ref-1 expression after SCI. This study suggests that anti-CD11d mAb treatment significantly reduces intraspinal free radical formation after SCI, thereby reducing protein and DNA oxidative damage. These effects likely underlie tissue preservation and improved neurological function resulting from the mAb treatment.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2003

Peroxynitrite generated in the rat spinal cord induces oxidation and nitration of proteins: reduction by Mn (III) tetrakis (4-benzoic acid) porphyrin.

To determine whether peroxynitrite at the concentration and duration present after spinal cord injury induces protein oxidation and nitration in vivo, the peroxynitrite donor 3-morpholinosydnonimine (SIN-1) was administered into the gray matter of the rat spinal cord for 5 hr. The cords were removed at 6, 12, 24, and 48 hr after SIN-1 exposure, immunohistochemically stained with antibodies to dinitrophenyl (DNP) and nitrotyrosine (Ntyr), markers of protein oxidation and nitration, respectively, and the immunostained neurons were counted. The percentages of DNP-positive (P = 0.023-0.002) and Ntyr-positive (P < 0.001 for all) neurons were significantly higher in the SIN-1-exposed groups than in the ACSF controls at each time, suggesting that peroxynitrite induced intracellular oxidation and nitration of proteins. The percentages of DNP- and Ntyr-positive neurons were not significantly different over time in either SIN-1- or ACSF-exposed groups (P = 0.20-1.00). The percentage of DNP-positive neurons was 7.6 +/- 3% to 12 +/- 4.2% at 6-24 hr, and it was 14 +/- 2% to 19 +/- 2% at 6-24 hr for Ntyr-positive neurons after SIN-1-exposure, whereas both ranged over 2-3% in ACSF controls. Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP, a broad-spectrum scavenger of reactive species) significantly reduced the percentages of DNP- and Ntyr-positive neurons (P = 0.04 and 0.002, respectively) compared to a SIN-1-exposed, untreated group at 24 hr after SIN-1 exposure. There were no significant differences between MnTBAP-treated and ACSF controls (P = 0.7 for DNP and 0.2 for Ntyr). These results further demonstrate peroxynitrite-induced protein oxidation and nitration and the efficiency of MnTBAP in scavenging peroxynitrite.

2,4-Dinitrophenol↗

PubMed2003

Redistribution of neurofilaments and accumulation of beta-amyloid protein after brain injury by rotational acceleration of the head.

Rotational acceleration of the head, as occurs in falls, car crashes, and sport injuries, may result in diffuse brain damage, with acute and chronic neurological and psychiatric symptoms. The present study addresses the effects of rotational trauma on the neuronal cytoskeleton, which stabilizes perikaryal, dendritic and axonal shape and function. The study focuses upon the distribution of (1) the phosphorylated form of the heavy neurofilament subunit, (2) the light neurofilament subunit, and (3) beta-amyloid, a marker for brain injury. While normally restricted to axons, the phosphorylated heavy neurofilament subunits were drastically decreased in the axons after rotational trauma. Instead, they accumulated in the neuronal perikarya, normally devoid of the phosphorylated subunit. This alteration was seen, not only in the cerebral cortex, but also in the hippocampus, the cervical spinal cord, the cerebellum, the cranial nerves and the pyramidal tract. The distribution of the light subunit of neurofilaments was also altered post trauma. Only a weak beta-amyloid immunoreactivity was detected in the brains of control animals. Promptly after the trauma, a large number of beta-amyloid positive neurons appeared. Intensely co-localized immunoreactivity for the light subunit of neurofilaments and of beta-amyloid was seen 3 days after the rotational trauma axons of in the subcortical white matter and in the granule cell layer of the dentate gyrus as well as in neurons of the hypoglossal nucleus. The reported alterations in the central nervous system neurons are similar to those in the human brain after closed head injury and in chronic degenerative diseases. Regions of importance for social behavior, memory and body movement were affected.

Acceleration↗

PubMed2002

Exposure to short-lasting impulse noise causes neuronal c-Jun expression and induction of apoptosis in the adult rat brain.

Exposure to impulse noise, above a certain intensity, is harmful to auditory function. Effects of impulse noise on the central nervous system (CNS) are largely unexplored, and there is little information on critical threshold values and time factors. We have recently shown that neurofilament proteins are affected in the cerebral cortex and the hippocampus. Now we show that impulse noise induces expression of the immediate early gene c-Jun products, proposed to play a role in the initiation of neuronal death, and apoptosis as revealed by TUNEL staining. Rat brains were investigated immunohistochemically 2 h to 21 days after exposure to impulse noise of 198 dB or 202 dB. c-Jun was expressed in neuronal perikarya in layers II-VI of the temporal cortex, the cingulate and the piriform cortices at 2 h to 21 days after both exposure levels. Granule neurons of the dentate gyrus and the CA1-3 in the hippocampus pyramidal neurons were similarly affected. The elevated expression of c-Jun products remained high at all postexposure times. TUNEL staining was positive among the same nerve cell populations 6 h after exposure and persisted even at 7 days at both exposure levels.

Animals↗

PubMed2002

Expression of c-Fos and c-Myc and deposition of beta-APP in neurons in the adult rat brain as a result of exposure to short-lasting impulse noise.

There is increasing evidence that impulse noise causes brain damage, but little is known about the mechanisms and extent of the response. Here, rat brains were investigated immunohistochemically for the expression of c-Fos, c-Myc, and beta-APP during the first 3 weeks postexposure to impulse noise of 198 or 202 dB. The expression of c-Fos and c-Myc increased at 2 h after exposure in neurons of the cerebral cortex, thalamus, and hippocampus, and this c-Fos immunoreactivity remained elevated for the entire observation period. The c-Myc immunoreactivity peaked at 18 h in both neurons and astrocytes but returned to control levels at 7 days. Abnormal deposition of beta-APP was evident within 6 h in the same brain regions. The beta-APP immunoreactivity was most prominent at 18 h and remained increased over the 21-day period assessed. The observed effects were similar to those described in humans following traumatic brain injury and in Alzheimer's disease. We conclude that impulse noise influences the brain in a fashion similar to that in cases with progressive CNS degeneration.

Amyloid beta-Protein Precursor↗