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Biomedical subjects

K Zhang

Publications and source records attributed to K Zhang.

At least 19 recordsLinked to original sources
PubMed2007

Receptor-mediated internalization of chelator-PNA-peptide hybridization probes for radioimaging or magnetic resonance imaging of oncogene mRNAs in tumours.

Early external detection of cancer gene activity might enable early treatment of cancer and might reduce cancer mortality. We hypothesized that oncogene mRNA overexpressed at thousands of copies per malignant cell in a zone of transformed cells could be imaged externally by scintigraphic imaging, PET (positron emission tomography) or MRI (magnetic resonance imaging) with PNA (peptide nucleic acid) hybridization probes that include chelators for metal cations and a cyclized peptide analogue of IGF-1 (insulin-like growth factor 1), D(Cys-Ser-Lys-Cys), to mediate internalization by IGF1R (IGF-1 receptor) overexpressed on cancer cells. We observed that human MCF7 breast cancer cells that overexpress IGF1R efficiently internalized fluorescein-chelator-PNA-D(Cys-Ser-Lys-Cys) to the cytoplasm, but not with D(Cys-Ala-Ala-Cys). Scintigraphic imaging of MCF7 xenografts in immunocompromised mice revealed that CCND1 and MYC [(99m)Tc]chelator-PNA-D(Cys-Ser-Lys-Cys) probes yielded xenograft. PET imaging with [(64)Cu]chelator-PNA-D(Cys-Ser-Lys-Cys) yielded stronger signals. Scintigraphic imaging of human AsPC1 pancreas cancer xenografts with [(99m)Tc]chelator-KRAS PNA-D(Cys-Ser-Lys-Cys) yielded strong xenograft signals. Stronger xenograft image intensities were obtained by PET imaging of [(64)Cu]chelator-KRAS PNA-D(Cys-Ser-Lys-Cys). MRI required extension of chelator-polydiamidopropanoate dendrimers from the N-termini of the PNA probes to increase the number of contrast paramagnetic gadolinium (III) cations per probe. These results provide a basis for detection of oncogene activity in tissues from outside the body by hybridization with metal-chelator-PNA-peptides that are selectively internalized by cancer cells.

Animals↗
PubMed2006

Colloidal particles at a nematic-isotropic interface: effects of confinement.

When captured by a flat nematic-isotropic interface, colloidal particles can be dragged by it. As a result spatially periodic structures may appear, with the period depending on particle mass, size, and interface velocity (J.L. West, A. Glushchenko, G.X. Liao, Y. Reznikov, D. Andrienko, M.P. Allen, Phys. Rev. E 66, 012702 (2002)). If liquid crystal is sandwiched between two substrates, the interface takes a wedge-like shape, accommodating the interface-substrate contact angle and minimizing the director distortions on its nematic side. Correspondingly, particles move along complex trajectories: they are first captured by the interface and then "glide" towards its vertex point. Our experiments quantify this scenario, and numerical minimization of the Landau-de Gennes free energy allows for a qualitative description of the interfacial structure and the drag force.

Anisotropy↗
PubMed2006

Observation of Psi(3770)-->gammachi(c1)-->gammagammaJ/Psi.

From e(+)e(-) collision data acquired with the CLEO detector at the Cornell Electron Storage Ring, we observe the non-DD(_) decay Psi(3770))-->gammachi(c1) with a statistical significance of 6.6 standard deviations, using the two-photon cascades to J/Psi and J/Psi-->l(+)l(-). We determine sigma(e(=)e(-)-->Psi(3770))xBeta(Psi(3770)-->gammachi(c1))=(18.0 +/- 3.3 +/- 2.5) pb and branching fraction Beta(Psi(3770)-->gammachi(c1)=(2.8 +/- 0.5+/-0.4) x 10(-3). We set 90% C.L. upper limits for the transition to chi(c2) (chi(c0)): sigma x Beta<5.7 pb (<282 pb) and Beta<0.9 x 10(-3) (<44 x 10(-3)). We also determine Gamma(Psi(3770)gammachi(c1))/Gamma(Psi(3770)-->pi(+)pi(-)J/Psi)=1.5 +/- 0.3 +/- 0.3 (>1.0 at 90% C.L.), which bears upon the interpretation of X(3872).

Journal Article↗
PubMed2006

Charmonium Decays of Y(4260), psi(4160), and psi(4040).

Using data collected with the CLEO detector operating at the CESR e+e- collider at sqrt[s]=3.97-4.26 GeV, we investigate 15 charmonium decay modes of the psi(4040), psi(4160), and Y(4260) resonances. We confirm, at 11 sigma significance, the BABAR Y(4260)-->pi+pi- J/psi discovery, make the first observation of Y(4260)--> pi(0)pi(0) J/psi (5.1 sigma), and find the first evidence for Y(4260)-->K+K- J/psi(3.7 sigma). We measure e+e- cross sections at sqrt[s]=4.26 GeV as sigma(pi+pi- J/psi)=58(+12)(-10)+/-4 pb, sigma(pi(0)pi(0) J/psi)=23(+12)(-8)+/-1 pb, and sigma(K+K- J/psi)=9(+9)(-5)+/-1 pb, in which the uncertainties are statistical and systematic, respectively. Upper limits are placed on other decay rates from all three resonances.

Journal Article↗
PubMed2006

Measurements of the exclusive decays of the upsilon(5S) to meson final states and improved B(s)* mass measurement.

Using 420 pb(-1) of data collected on the upsilon(5S) resonance with the CLEO III detector, we reconstruct B mesons in 25 exclusive decay channels to measure or set upper limits on the decay rate of upsilon(5S) into B meson final states. We measure the inclusive B cross section to be sigma(upsilon(5S) --> BB(X)) = (0.177 +/- 0.030 +/- 0.016) nb and make the first measurements of the production rates of sigma(upsilon(5S) --> B*B*) = (0.131 +/- 0.025 +/- 0.014) nb and sigma(upsilon(5S) --> BB*) = (0.043 +/- 0.016 +/- 0.006) nb, respectively. We set 90% confidence level limits of sigma(upsilon(5S) -->BB) < 0.038 nb, sigma(upsilon(5S) --> B(*)B(*)pi) < 0.055 nb and sigma(upsilon(5S) --> BBpipi) < 0.024 nb. We also extract the most precise value of the B(s)* mass to date, M(B(s)*) = (5411.7 +/- 1.6 +/- 0.6) MeV/c2.

Journal Article↗
PubMed2006

Measurement of sigma(e+e- -->psi(3770)-->hadrons) at Ec.m.=3773 MeV.

We measure the cross section for e+e- -->psi(3770) -->hadrons at Ec.m.=3773 MeV to be (6.38+/-0.08(+0.41)(-0.30) nb using the CLEO detector at the CESR e+e- collider. The difference between this and the e+e- -->psi(3770) -->DD cross section at the same energy is found to be (-0.01+/-0.08(+0.41)(-0.30) nb. With the observed total cross section, we extract Gamma(ee)(psi(3770))=(0.204+/-0.003(+0.041)(-0.027) keV. Uncertainties shown are statistical and systematic, respectively.

Journal Article↗
PubMed2006

New measurements of Cabibbo-suppressed decays of mesons with the CLEO-c detector.

Using of data collected with the CLEO-c detector, we report on first observations and measurements of Cabibbo-suppressed decays of D mesons in the following six decay modes: pi+ pi- pi0 pi0, pi+ pi+ pi- pi- pi0, pi+ pi0 pi0, pi+ pi+ pi- pi0, eta pi0, and omega pi+ pi-. Improved branching fraction measurements in eight other multipion decay modes are also presented. The measured D --> pi pi rates allow us to extract the ratio of isospin amplitudes A(DeltaI = (3/2) / A(DeltaI = (1/2)) = 0.420 +/- 0.014(stat) +/- 0.016(syst) and the strong phase shift of delta1 = (86.4 +/- 2.8 +/- 3.3) degrees, which is quite large and now more precisely determined.

Journal Article↗
PubMed2006

Structure of the carboxy-terminal PH domain of pleckstrin at 2.1 Angstroms.

Pleckstrin is an important intracellular protein involved in the phosphoinositide-signalling pathways of platelet activation. This protein contains both N- and C-terminal pleckstrin-homology (PH) domains (N-PH and C-PH). The crystal structure of C-PH was solved by molecular replacement and refined at 2.1 Angstroms resolution. Two molecules were observed within the asymmetric unit and it is proposed that the resulting dimer interface could contribute to the previously observed oligomerization of pleckstrin in resting platelets. Structural comparisons between the phosphoinositide-binding loops of the C-PH crystal structure and the PH domains of DAPP1 and TAPP1, the N-terminal PH domain of pleckstrin and a recently described solution structure of C-PH are presented and discussed.

Amino Acids↗
PubMed2006

Search for exclusive multibody non- decays at the resonance.

Using data collected at the psi(3770) resonance with the CLEO-c detector at the Cornell e+e- storage ring, we present searches for 25 charmless decay modes of the psi(3770), mostly multibody final states. No evidence for charmless decays is found.

Journal Article↗
PubMed2006

Role of heteroatoms in activated carbon for removal of hexavalent chromium from wastewaters.

Heteroatoms are elements including sulfur, nitrogen, oxygen and hydrogen which are found on the surface of activated carbons. This study investigated the surface modification arising from heteroatoms bonding to carbon aromatic rings within the activated carbon and their corresponding influence on the chromium adsorption process. Activated carbons were prepared from bagasse by physical. Chromium removal capacities of these activated carbons by adsorption and reduction were determined. Models which related the chromium adsorption and reduction capacities of activated carbons to carbon acidity and heteroatom site concentrations were established using multi-variable linear regression method. It was found the individual heteroatoms contributed separately to the basicity of the carbon which in turn determined the mechanism by which chromium was removed from solution. The surface areas of the carbons were also observed to influence the adsorption and reduction of chromium. These understandings provide the fundamental method of optimising chromium removal through suitable control of carbon surface chemistry and textural properties.

Carbon↗
PubMed2006

Protein folding in the endoplasmic reticulum and the unfolded protein response.

In all eukaryotic cells, the endoplasmic reticulum (ER) is an intracellular organelle where folding and assembly occurs for proteins destined to the extracellular space, plasma membrane, and the exo/endocytic compartments (Kaufman 1999). As a protein-folding compartment, the ER is exquisitely sensitive to alterations in homeostasis, and provides stringent quality control systems to ensure that only correctly folded proteins transit to the Golgi and unfolded or misfolded proteins are retained and ultimately degraded. A number of biochemical and physiological stimuli, such as perturbation in calcium homeostasis or redox status, elevated secretory protein synthesis, expression of misfolded proteins, sugar/glucose deprivation, altered glycosylation, and overloading of cholesterol can disrupt ER homeostasis, impose stress to the ER, and subsequently lead to accumulation of unfolded or misfolded proteins in the ER lumen. The ER has evolved highly specific signaling pathways called the unfolded protein response (UPR) to cope with the accumulation of unfolded or misfolded proteins. Elucidation of the molecular mechanisms by which accumulation of unfolded proteins in the ER transmits a signal to the cytoplasm and nucleus has led to major new insights into the diverse cellular and physiological processes that are regulated by the UPR. This chapter summarizes how cells respond to the accumulation of unfolded proteins in the cell and the relevance of these signaling pathways to human physiology and disease.

Animals↗
PubMed2006

Experimental study on in vitro tumor cell killing by focused bi-frequency ultrasound activated hematoporphyrin derivatives.

OBJECTIVE: As ultrasound has become an important therapeutic technique on tumor, in order to find the cell-killing effect of focused bi-frequency ultrasound activated hematoporphyrin derivatives, experimental study was processed in vitro. METHODS: Tumor cells K562 and SW-480 were killed by focused bi-frequency ultrasound activated hematoporphyrin (Hp) derivatives under optimized ultrasonic parameters and the cell-killing effect was tested by MTT (Thiazolyl blue: 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide) technique. RESULTS: The lower frequency (0.6 MHz) was better than the higher (1.1 MHz) in activating hematoporphyrin derivatives; the bi-frequency was better than mono-frequency, and the cell-killing efficiency was 2-3 times of sum of the two kinds of ultrasounds which constitute bi-frequency. Incubation for the 16 h was better than 4 h after the cells exposed to the ultrasound. CONCLUSION: The method of killing tumor cells by focused bi-frequency ultrasound activated hematoporphyrin derivatives is presented and evaluated in this paper.

Apoptosis↗
PubMed2006

Segmental axonopathy of Merino sheep in New Zealand.

AIM: To investigate an axonopathy of Merino sheep that caused progressive hindlimb ataxia and slight to moderate paresis, with the purpose of understanding its pathogenesis. METHODS: Tissues were fixed in buffered paraformaldehyde or paraformaldehyde and glutaraldehyde, processed into wax and epoxy resin, respectively, and examined by light and electron microscopy. Fresh frozen spinal cord and trigeminal nerve roots were subjected to homogenisation, centrifugation and two-dimensional electrophoresis. Selected protein spots were identified using matrix-assisted laser desorption ionisation (MALDI) mass spectrometry. RESULTS. By light microscopy, there were large pale foamy spheroidal axonal swellings affecting peripheral as well as central axons. By electron microscopy, these were shown to contain many membrane-bound vesicles. The main abnormalities in expressed proteins involved cytoskeletal elements and myosin heavy chain, the latter interpreted as associated with the molecular motor myosin Va. CONCLUSIONS: The disorder is the same as that described in Merinos in Australia as segmental axonopathy, and believed to have an inherited aetiology. The lesions and protein changes indicate abnormalities of the cytoskeleton, its relationship with the myelin sheath, and myosin Va molecular motor. The consequence appears to be abnormal axonal transport and inability to maintain the integrity of axons and their myelin sheaths.

Animals↗
PubMed2006

A novel single-nucleotide polymorphism of the Fcgamma receptor IIIa gene is associated with genetic susceptibility to systemic lupus erythematosus in Chinese populations: a family-based association study.

BACKGROUND: Systemic lupus erytematosus (SLE) is characterized by the presence of various autoantibodies and the deposition of immune complexes which are cleared by Fcgamma receptors. OBJECTIVES: Family-based association analysis was performed to investigate whether the FCGR3A-72S/R and FCGR3A-270T/R polymorphisms are risk factors for SLE in a Chinese population. METHODS: In total, 119 patients with SLE from 95 nuclear families, aged 14-78 years, who met the American College of Rheumatology 1997 criteria were recruited, as were 316 family members of these patients. We studied two single-nucleotide polymorphisms (SNPs) encoding nonsynonymous substitution in the FCGR3A gene with respect to genetic susceptibility to SLE in a collection of 435 subjects from 95 nuclear families. We performed the genotyping using PCR restriction fragment length polymorphism. RESULTS: Our results showed that FCGR3A-72R/S have an excess of transmission of the R allele from heterozygous parents to affected offspring (transmission disequilibrium test chi2 = 9.30, P = 0.0032). Univariate (single-marker) family-based association tests demonstrated that a variant allele at SNP rs403016 of the FCGR3A gene was significantly associated with genetic susceptibility to SLE (exon 3, Z = 2.5444, P = 0.01097) in an additive model. The R and S allele frequencies were 39.4% and 60.6%, respectively. The frequencies of FCGR3A 72R/R, R/S and SS genotypes were 9.1%, 60.6% and 30.3%, respectively. However, the FCGR3A-270T/S SNP was not found in this Chinese population. CONCLUSION: This study suggests a linkage disequilibrium of the FCGR3A-72R/S SNP with SLE, and supports the notion that a novel polymorphism of the FCGR3A-72R/S SNP is associated with genetic susceptibility to SLE in Chinese populations.

Adolescent↗
PubMed2006

A novel locus on 19q13 associated with autosomal-dominant macular dystrophy in a large Greek family.

OBJECTIVE: To describe the clinical features of and genetic locus associated with autosomal-dominant macular dystrophy (MCDR5) in a large Greek family. METHODS: 26 members of a single family underwent clinical examinations and venepuncture. A genomewide linkage scan using 400 microsatellite markers distributed with an average spacing of 10 cM throughout the human genome. RESULTS: 14 members of the study family exhibited clinical features of the disease including decreased central vision and macular abnormalities in the posterior pole of the retina. Analysis of loci known to be associated with macular dystrophy did not show positive linkage. A genomewide linkage scan showed linkage to chromosome 19q, with a two-point maximum LOD score of 5.809 at theta = 0 between the disease and marker locus D19S412. On the basis of recombination events, the disease interval was localised between markers D19S420 and D19S540 on chromosome 19q, at a span of about 3.8 cM, in an area known to contain 120 known genes/transcripts. Eleven of these genes/transcripts were sequenced, and no disease-causing mutation was identified. CONCLUSIONS: This study describes a new locus on 19q associated with autosomal-dominant macular dystrophy, designated as MCDR5. Additional study of other family members will be necessary to further narrow the interval and identify the responsible gene. The study of MCDR5 will aid in elucidation of the underlying pathogenic mechanisms for this and other macular diseases, including age-related macular degeneration.

Adolescent↗
PubMed2006

Growth of aligned ZnO nanorods.

Growth of high-density and aligned ZnO nanorods on ZnO film substrate has been demonstrated using vapor-transport of thermally evaporated Zn metal powders followed by condensation. Morphological studies show that the nanorods grow preferentially from a hexagonal ZnO base with a uniform hexagonal structure following three-dimensional island-like growth mechanism. Structural and spectroscopic properties clearly indicate that the nanorods are relatively good and defect-free in quality. These nanorods have potential for technological implications.

Crystallization↗
PubMed2006

Effects of phenylephrine on transplanted submandibular gland.

Autotransplantation of the submandibular gland is a potential treatment for severe kerato-conjunctivitis sicca. However, one of the major barriers to this procedure is that secretions from the transplanted gland decrease shortly after the operation, which may lead to obstruction of Wharton's duct, or even to transplantation failure. Using a rabbit model, we investigated whether phenylephrine could improve the secretion from the transplanted gland. We found that phenylephrine treatment significantly reversed the decrease in salivary secretion after transplantation, enhanced the expressions of alpha1A-, alpha1B-, and alpha1D-adrenoceptor mRNA, and ameliorated atrophy of acinar cells. Furthermore, phenylephrine also induced translocation of aquaporin-5 from the cytoplasm to the apical membrane, and increased the levels of phospho-ERK1/2, ERK1/2, phospho-PKCzeta, and PKCzeta in the transplanted gland. These results indicate that phenylephrine treatment moderates structural injury and improves secretory function in the transplanted submandibular gland through promoting alpha1-adrenoceptor expression and post-receptor signal transduction.

Adrenergic alpha-Agonists↗