Biomedical subjects

J Z Wang

Publications and source records attributed to J Z Wang.

At least 19 recordsLinked to original sources

PubMed2006

Dose escalation to combat hypoxia in prostate cancer: a radiobiological study on clinical data.

Earlier studies have demonstrated that hypoxic regions exist in human prostate cancer and the degree of hypoxia correlates with the treatment outcome of radiotherapy. Using the concept of the clinical oxygen enhancement ratio (COER), the linear-quadratic (LQ) model was extended to account for the effect of tumour hypoxia. The clinical data collected at the Fox Chase Cancer Center for prostate cancer were analysed based on the LQ model as well as the tumour control probability (TCP) model. The LQ and TCP parameters (alpha = 0.15 Gy (-1), alpha/beta = 3.1 Gy and the number of clonogens K = 10(6) approximately 10(7) cells) determined in earlier studies were used to derive the COER for prostate cancer: COER = 1.4 with a standard confidence interval (CI) of (1.2, 1.8). The result is consistent with the in vitro OER measurements of human tumour cell lines under chronic hypoxia conditions. This implies that a higher dose is needed to overcome tumour hypoxia. For prostate tumours, the prescription dose required to overcome tumour hypoxia is 165 Gy (CI: 153 approximately 186 Gy) for permanent 125I implants and 88 Gy (CI: 74 approximately 118 Gy) in 2 Gy fractions for external-beam radiotherapy. The impact of LQ parameters on the calculations of COER and dose escalation was discussed. This study provides a preliminary estimate of the dose escalation needed to overcome tumour hypoxia based on clinical data. More clinical data with better statistics and longer follow-up time are required to further tune the radiobiological modelling of hypoxia for prostate cancer.

Brachytherapy↗

PubMed2006

Dose escalation of three-dimensional conformal radiotherapy for locally recurrent nasopharyngeal carcinoma: a prospective randomised study.

AIMS: To investigate prospectively the feasibility and efficacy of dose escalation using three-dimensional conformal radiotherapy (3D-CRT) boost technique for locally recurrent nasopharyngeal carcinoma (NPC) in a randomised study. MATERIALS AND METHODS: Thirty-six patients with locally recurrent NPC (>6 months interval from previous radical radiotherapy, no cervical lymph-node involvement and no distant metastasis) were enrolled. Treatment included conventional external-beam radiotherapy to 54 Gy, followed by a 3D-CRT boost to the gross tumour region. Patients were randomised to three boost dose levels: 16 Gy, 20 Gy and 24 Gy for groups I, II and III, respectively, with 12 patients in each group. All boost doses were delivered in 4-Gy fractions and 3 fractions per week. Median follow-up was 27 months (range 14-44 months). RESULTS: Three-year, local-recurrence-free survival rate was significantly higher (72%) for the high-dose group III than for groups I and II (37% and 28%, respectively, P = 0.047). No significant difference was found in the 3-year overall survival rate among the three groups (72%, 59% and 82% for groups I, II and III, respectively). Three-year distant metastases rates were 17%, 0% and 18%, respectively. Skull-base invasion (P = 0.017) and pathology (P = 0.0006) correlated with overall survival. Treatment was well tolerated and no significant difference was observed among the three groups in acute and late toxicities (grade III toxicity is minimal: 17%, 17%, 0% of oral mucositis and 25%, 17%, 17% of nasopharyngeal mucositis in groups I, II, III, respectively, and 8% leukocytopenia only in group II; no grade IV toxicity occurred in any of the groups except for a fatal bleeding in group III). CONCLUSIONS: Re-irradiation with high-dose 3D-CRT boost technique results in high local control rate and acceptable toxicity in patients with recurrent NPC. Dose escalation to the boost volume to 78 Gy (54 Gy + 24 Gy boost) results in improved recurrence-free survival compared with lower doses.

Adult↗

PubMed2006

Electrochemical hydrogen storage in single-walled carbon nanotube paper.

Single-walled carbon nanotube (SWNT) papers were successfully prepared by dispersing SWNTs in Triton X-100 solution, then filtered by PVDF membrane (0.22 microm pore size). The electrochemical behavior and the reversible hydrogen storage capacity of single-walled carbon nanotube (SWNT) papers have been investigated in alkaline electrolytic solutions (6 N KOH) by cyclic voltammetry, linear micropolarization, and constant current charge/discharge measurements. The effect of thickness and the addition of carbon black on hydrogen adsorption/desorption were also investigated. It was found that the electrochemical charge-discharge mechanism occurring in SWNT paper electrodes is somewhere between that of carbon nanotubes (physical process) and that of metal hydride electrodes (chemical process), and consists of a charge-transfer reaction (Reduction/Oxidation) and a diffusion step (Diffusion).

Absorption↗

PubMed2005

The requirements and mechanism for capsid assembly and budding of bovine foamy virus.

Little is known about assembly of non-primate foamy virus (FV) such as bovine foamy virus (BFV). To help determine the requirements for assembly of BFV, we constructed BFV-Gag expression plasmids containing all or part of the gag gene, with or without modification by addition of myristate (Myr). Each construct was transfected alone, and with pFenv, into Sf-9 insect cells. The results showed that only the entire Gag could transit through nucleus, which is required for BFV viral assembly in the cytoplasm. Unlike other retroviruses (but like primate foamy viruses), BFV requires the coexpression of the Env protein for viral particle budding. In the case of BFV, this occurs at the plasma membrane rather than the endoplasmic reticulum (ER), due to lack of a functional ER retrieval signal (ERRS). The results also showed that addition of a Myr-membrane targeting signal to the C-terminus of Gag could restore the budding from plasma membrane, implying that Myr-membrane targeting signal could substitute for Env protein in budding.

Animals↗

PubMed2005

Enhancement of ionic conductivity of PEO based polymer electrolyte by the addition of nanosize ceramic powders.

The ionic conductivity of polyethylene oxide (PEO) based solid polymer electrolytes (SPEs) has been improved by the addition of nanosize ceramic powders (TiO2 and AL2O3). The PEO based solid polymer electrolytes were prepared by the solution-casting method. Electrochemical measurement shows that the 10 wt% TiO2 PEO-LiClO4 polymer electrolyte has the best ionic conductivity (about 10(-4) S cm(-1) at 40-60 degrees C). The lithium transference number of the 10 wt% TiO2 PEO-LiClO4 polymer electrolyte was measured to be 0.47, which is much higher than that of bare PEO polymer electrolyte. Ac impedance testing shows that the interface resistance of ceramic-added PEO polymer electrolyte is stable. Linear sweep voltammetry measurement shows that the PEO polymer electrolytes are electrochemically stable in the voltage range of 2.0-5.0 V versus a Li/Li+ reference electrode.

Aluminum Oxide↗

PubMed2004

Dewetting of conducting polymer inkjet droplets on patterned surfaces.

The manufacture of high-performance electronic devices with micrometre or even submicrometre dimensions by solution processing and direct printing, requires the ability to control accurately the flow and spread of functional liquid inks on surfaces. This can be achieved with the help of surface-energy patterns causing inks to be repelled and dewetted from pre-defined regions of the substrate. To exploit this principle for the fabrication of submicrometre device structures, a detailed understanding of the factors causing ink droplets to dewet on patterned surfaces is required. Here, we use hydrophobic surface-energy barriers of different geometries to study the influence of solution viscosity, ink volume, and contact angle on the process of dewetting of inkjet-printed droplets of a water-based conducting polymer. We demonstrate polymer field-effect transistor devices with channel length of 500 nm fabricated by surface-energy-assisted inkjet printing.

Hydrophobic and Hydrophilic Interactions↗

PubMed2003

Inhibition of protein phosphatase 2A- and protein phosphatase 1-induced tau hyperphosphorylation and impairment of spatial memory retention in rats.

Tau hyperphosphorylation leads to formation of paired helical filament/neurofibrillary tangles, the hallmark lesion seen in Alzheimer's disease (AD) brain. An imbalanced regulation in protein kinases and protein phosphatases in the affected neurons is proposed to be a reasonable causative factor to the disease process. To verify the hypothesis, we have injected in the present study calyculin A, a potent and specific inhibitor of protein phosphatase (PP) 2A and PP1, into rat hippocampus bilaterally, thus reproduced an Alzheimer's-like deficiency in dephosphorylation system. It was found that calyculin A-injected rats developed lesions in spatial memory retention in Morris water maze test. At mean time, tau was hyperphosphorylated at Ser396/Ser404 (PHF-1) and Ser-262/Ser-356 (12E8) sites determined both by immunohistochemistry and Western blot. It is implicated that (1) PP2A and PP1 participate in the in vivo regulation of tau phosphorylation, and down-regulation of the two phosphatases will result in tau hyperphosphorylation; (2) hyperphosphorylation of tau at PHF-1 and 12E8 sites might be crucial to affect spatial memory in AD.

Animals↗

PubMed2002

Measurements of cosmic-ray low-energy antiproton and proton spectra in a transient period of solar field reversal.

The energy spectra of cosmic-ray low-energy antiprotons ( *p's) and protons ( p's) have been measured by BESS in 1999 and 2000, during a period covering reversal at the solar magnetic field. Based on these measurements, a sudden increase of the *p/p flux ratio following the solar magnetic field reversal was observed, and it generally agrees with a drift model of the solar modulation.

Journal Article↗

PubMed2001

Anti-nociceptive effect of neuropeptide Y in periaqueductal grey in rats with inflammation.

Experimental inflammation was induced by subcutaneous injection of carrageenan into the left hindpaw of rats. Intra-periaqueductal grey (PAG) injection of 0.02 or 0.1 nmol of neuropeptide Y (NPY), but not 0.004 nmol, induced significant increases in hindpaw withdrawal latency (HWL) to thermal and mechanical stimulation in rats with inflammation. Furthermore, the anti-nociceptive effect of NPY was blocked partly by following intra-PAG injection of the Y1 receptor antagonist NPY28-36. The results demonstrated that NPY plays an anti-nociceptive role in PAG in rats with inflammation, in which Y1 receptor is involved.

Animals↗

PubMed2001

Wavelets and imaging informatics: a review of the literature.

Modern medicine is a field that has been revolutionized by the emergence of computer and imaging technology. It is increasingly difficult, however, to manage the ever-growing enormous amount of medical imaging information available in digital formats. Numerous techniques have been developed to make the imaging information more easily accessible and to perform analysis automatically. Among these techniques, wavelet transforms have proven prominently useful not only for biomedical imaging but also for signal and image processing in general. Wavelet transforms decompose a signal into frequency bands, the width of which are determined by a dyadic scheme. This particular way of dividing frequency bands matches the statistical properties of most images very well. During the past decade, there has been active research in applying wavelets to various aspects of imaging informatics, including compression, enhancements, analysis, classification, and retrieval. This review represents a survey of the most significant practical and theoretical advances in the field of wavelet-based imaging informatics.

Algorithms↗

PubMed2001

Multiple forms of phosphatase from human brain: isolation and partial characterization of affi-gel blue nonbinding phosphatase activities.

Phosphatases extracted from a human brain were resolved into two main groups, namely affi-gel blue-binding phosphatases and affi-gel blue-nonbinding phosphatases. Affi-gel blue binding phosphatases were further separated into four different phosphatase activities, designated P1-P4, and described previously. In the present study we describe the affi-gel blue-nonbinding phosphatases which were separated into seven different phosphatase activities, designated P5-P11 by poly-(L-lysine)-agarose and aminohexyl Sepharose 4B chromatographies. These seven phosphatase activities were active toward nonprotein phosphoester. P7-P11 and to some extent P5 could also dephosphorylate a phosphoprotein. They displayed different enzyme kinetics. On the basis of activity peak, the apparent molecular mass as estimated by Sephadex G-200 column chromatography for P5 was 49 kDa; P6, 32 kDa; P7, 150 kDa; P8, 250 kDa; P9, 165 kDa; P10, 90 kDa and P11, 165 kDa. Immunoblot analysis indicated that P8-P11 may belong to PP2B family, whereas P7 may associate with PP2A. The phosphatases P7-P11 were found to be effective in the dephosphorylation of Alzheimer's disease abnormally hyperphosphorylated tau. The resulting dephosphorylated tau regained its activity in promoting the microtubule assembly, suggesting that P7-P11 might regulate the phosphorylation of tau protein in the brain.

Aged↗

PubMed2001

[Alzheimer-like protein phosphatase deficiency leads to abnormal phosphorylation and accumulation of neurofilaments].

OBJECTIVE: To explore the effect of Alzheimer-like protein phosphatase deficiency on neurofilament phosphorylation. METHODS: Cell culture, light microscopy, immunocytochemistry and biochemistry techniques were used to make a phosphatase deficient cell model, to detect cell morphology, neurofilament phosphorylation and distribution, cell viability and activity. RESULTS: Non-phosphorylated neurofilament recognized by SMI32 was detected both in cell body and cell processes, it was extremely enriched in cell bodies; Phosphorylated neurofilament bound to SMI34 was mainly determined in cell processes and cell surface. After treatment with okadaic acid (OA), non-phosphorylation-dependent antibodies SMI32 staining was significantly decreased in the cell body, whereas phosphorylated neurofilament reacted with SMI34 was strikingly increased in immunocytochemistry and Western blot, and prominently accumulated to the same cell location. Accompanied with hyper-phosphorylation and accumulation of neurofilament, dose dependent cell toxicity was observed by okadaic acid treatment. CONCLUSION: Deficiency in protein phosphatase induces in neuroblastoma cell line, neurofilament phosphorylation and accumulation, which is involved in Alzheimer neurofibrillary degeneration.

Alzheimer Disease↗

PubMed2001

[Comparative study of the expression and phosphorylation of neurofilament proteins of brain gray matter in Alzheimer's disease].

OBJECTIVE: To explore the role of abnormal modification of neurofilament proteins (NFPs) in the pathogenesis of Alzheimer disease (AD), and the characteristics of NFPs in distribution and solubility. METHOD: Ultra-centrifugation and Western blot were utilized to isolate and analyze NF subunits. Ultra-centrifugation and Western blot were utilized to observe the effect of abnormal modification of neurofilament proteins (NFPs) on the characteristics of NFPs in distribution and solubility in the pathogenesis of Alzheimer disease. RESULTS: In human brain gray matter, NF subunits were mainly detected in particular fraction. Compared with Huntington's disease (HD), the content of NF subunits was increased in AD brain gray matter and the increased level of NF-H and NF-M were mainly in abnormal hyper-phosphorylate form. CONCLUSION: Abnormal phosphorylation and accumulation of NFPs are involved in pathology of AD brain.

Alzheimer Disease↗

PubMed2001

[The role of neuroimmunoregulation mobilized by enhancing immunologic function via hou hai acupoint antigen injection].

OBJECTIVE: To study the mechanism of neuroimmunoregulation which is triggered by enhancing immunologic function via Hou Hai acupoint antigen injection. METHODS: Immunohistochemical method, immunofluorometric method and RT-PCR were used to examine the different distribution of cytokine immunopositive cells in the brain and expression of cytokines in the spleen of the human IgG sensitized rats received acupoint, subcutaneous and normal rats antigen injections. RESULTS: In the areas of lateral hypothalamic nucleus (LH) and amygdaloid nuclear complex (AA), the distribution of cytokines immunopositive cells with acupoint injection group was significantly increased more than that in the subcutaneous injection group. But the expression of cytokines immunopositive cells both by the acupoint injection and the subcutaneous injection groups reached their peak value in similar time. Double-labelling results showed that the cytokine immunopositive cells were neurons. In the spleens, the expressions of cytokines, IL-2 and IFN, were significantly increased by acupoint injection more than subcutaneous injection. CONCLUSIONS: The time course of neuroimmunoregulation is similar in the immunized rats via both acupoint injection and subcutaneous injection of antigens. But the activity of neuroimmunoregulation is not the same in acupoint and subcutaneous injection groups. Neurons of the LH and AA are the main source of the neuroimmunomodulators. The effect of enhancing immunologic function via Hou Hai acupoint injection is may be more efficient to mobilize the activity of neuroimmunoregulation of immune-associated brain region than modulation of the immune system.

Acupuncture Points↗

PubMed2000

Antinociceptive effects induced by intra-periaqueductal grey administration of neuropeptide Y in rats.

Hindpaw withdrawal latency (HWL) to thermal and mechanical stimulation increased dose-dependently after intra-periaqueductal grey (PAG) injection of neuropeptide Y (NPY). Furthermore, the NPY-induced increases in HWLs were attenuated by intra-PAG injection of the Y1 receptor antagonist NPY28-36. The results demonstrated that NPY plays an important role in antinociception in PAG, in which Y1 receptor is involved in.

Analgesia↗

PubMed2000

Electrospray ionization mass spectra of amino acid phosphoramidates of adenosine.

Amino acid phosphoramidates of adenosine were synthesized and determined by positive and negative ion electrospray ionization mass spectrometry (ESI-MS) in conjunction with tandem mass spectrometry (MS/MS). The fragmentation pathways were investigated. In the positive ion mass spectra abundant characteristic fragment ions appeared, and many complementary ions were found. In the negative ion mass spectra only a few fragment ions were observed, and most of them contained phosphoryl groups. The results show that ESI-MS is a useful tool for structural determination of amino acid phosphoramidates of nucleosides.

Adenosine↗

PubMed2000

Mechanism of neurofibrillary degeneration and pharmacologic therapeutic approach.

Neurofibrillary degeneration is a key histopathological brain lesion of Alzheimer disease (AD) and related neurodegenerative disorders such as frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17), commonly referred to as tauopathies. Microtubule associated protein (MAP) tau, which is a major MAP of a normal mature neuron is abnormally hyperphosphorylated in tauopathies and is the major protein subunit of paired helical filaments (PHF)/straight filaments (SF) which accumulate in the soma (as neurofibrillary tangles) and dystrophic neurites (as neuropil threads and as dystrophic neurites surrounding the beta-amyloid core in neuritic plaques in AD) of the affected neurons. Unlike normal tau which stimulates assembly and stabilizes microtubules, the abnormally hyperphosphorylated tau inhibits assembly and disrupts microtubules. The abnormally hyperphosphorylated tau competes with tubulin/microtubules in associating with normal tau, MAP1 and MAP2. This sequestration of normal MAPs by the abnormal tau results in the breakdown of the microtubules. The association of the abnormal tau with normal tau and not with MAP1 or MAP2 results in the formation of tangles of tau filaments. All these toxic properties of the abnormally hyperphosphorylated tau are eliminated by its enzymatic dephosphorylation. Activities of phosphoseryl/phosphothreonyl protein phosphatases (PP)-2A and PP-1 which can dephosphorylate the abnormal tau to a normal-like state are compromised in AD brain. Dephosphorylation by PP-2A and PP-2B and to a lesser extent by PP-1 restores the normal microtubule assembly promoting activity in AD P-tau in vitro. Neurofibrillary tangles of PHF isolated from AD brain are also dissociated on in vitro dephosphorylation with PP-2A, and the tau released by this treatment can stimulate microtubule assembly. Thus, it appears that the abnormal hyperphosphorylation of tau leads to neurodegeneration through breakdown of the microtubule network and that the abnormal tau on association with normal tau forms neurofibrillary tangles of tau filaments i.e. PHF/SF. Increase in tau phosphatase activity is a promising approach to inhibit neurofibrillary degeneration and thereby the diseases characterized by this lesion.

Alzheimer Disease↗

PubMed2000

Multiple forms of phosphatase from human brain: isolation and partial characterization of affi-gel blue binding phosphatases.

Implication of protein phosphatases in Alzheimer disease led us to a systemic investigation of the identification of these enzyme activities in human brain. Human brain phosphatases eluted from DEAE-Sephacel with 0.22 M NaCl were resolved into two main groups by affi-gel blue chromatography, namely affi-gel blue-binding phosphatases and affi-gel blue-nonbinding phosphatases. Affi-gel blue-binding phosphatases were further separated into four different phosphatases, designated P1, P2, P3, and P4 by calmodulin-Sepharose 4B and poly-(L-lysine)-agarose chromatographies. These four phosphatases exhibited activities towards nonprotein phosphoester and two of them, P1 and P4, could dephosphorylate phosphoproteins. The activities of the four phosphatases differed in pH optimum, divalent metal ion requirements, sensitivities to various inhibitors and substrate affinities. The apparent molecular masses as estimated by gel-filtration for P1, P2, P3, and P4 were 97, 45, 42, and 125 kDa, respectively. P1 is markedly similar to PP2B from bovine brain and rabbit skeletal muscle. P4 was labeled with anti-PP2A antibody and may represent a new subtype of PP2A. P1 and P4 were also effective in dephosphorylating Alzheimer disease abnormally hyperphosphorylated tau (AD P-tau). The resulting dephosphorylated AD P-tau had its activity restored in promoting assembly of microtubules in vitro. These results suggest that P1 and P4 might be involved in the regulation of phosphorylation of tau in human brain, especially in neurodegenerative conditions like Alzheimer's disease which are characterized by the abnormal hyperphosphorylation of this protein.

Alzheimer Disease↗