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J Hu

Publications and source records attributed to J Hu.

At least 73 records · Page 4Linked to original sources
PubMed2003

Measurement of ep-->e' ppi+ pi- and baryon resonance analysis.

The cross section for the reaction ep-->e(')ppi(+)pi(-) was measured in the resonance region for 1.4<W<2.1 GeV and 0.5<Q2<1.5 GeV(2)/c(2) using the CLAS detector at Jefferson Laboratory. The data show resonant structures not visible in previous experiments. The comparison of our data to a phenomenological prediction using available information on N(*) and Delta states shows an evident discrepancy. A better description of the data is obtained either by a sizable change of the properties of the P13(1720) resonance or by introducing a new baryon state, not reported in published analyses.

Journal Article↗
PubMed2003

First measurement of transferred polarization in the exclusive ep-->e'K+Lambda--> reaction.

The first measurements of the transferred polarization for the exclusive e-->p-->e(')K+Lambda--> reaction have been performed at Jefferson Laboratory using the CLAS spectrometer. A 2.567 GeV beam was used to measure the hyperon polarization over Q2 from 0.3 to 1.5 (GeV/c)(2), W from 1.6 to 2.15 GeV, and over the full K+ center-of-mass angular range. Comparison with predictions of hadrodynamic models indicates strong sensitivity to the underlying resonance contributions. A nonrelativistic quark-model interpretation of our data suggests that the ssmacr; quark pair is produced with spins predominantly antialigned. Implications for the validity of the most widely used quark-pair creation operator are discussed.

Journal Article↗
PubMed2003

Sleep-deprived mice show altered cytokine production manifest by perturbations in serum IL-1ra, TNFa, and IL-6 levels.

Serum cytokine and chemokine levels were examined in mice following 36 h of sleep deprivation, or after exposure to a known physical stressor (rotational stress). Significant changes in inflammatory cytokines/chemokines (IL-1beta, TNFalpha, IL-1ra, IL-6, and MIP-1beta, MCP-1) were observed following each manipulation, but qualitative and quantitative differences were seen. Interestingly, only physical stress was associated with measured increases in serum corticosterone levels, and with independent evidence (using in vitro immune allostimulation) for a generalized immunosuppression secondary to the experimental manipulation. Our data suggest that altered cytokine production following sleep perturbation occurs by a different mechanism from that (HPA axis) commonly attributed to stress per se.

Acebutolol↗
PubMed2003

Comparative study of primary and recurrent ovarian serous carcinomas: comparative genomic hybridization analysis with a potential application for prognosis.

OBJECTIVES: The purpose of this study is to comparatively characterize genomic imbalances in primary and recurrent ovarian serous carcinomas and to identify genomic alterations that may be used as a marker for prognosis. METHODS: Twenty ovarian serous carcinomas were studied by comparative genomic hybridization (CGH). RESULTS: Genomic alterations were found in all of the tumors. The most common regions involving gain of DNA copy numbers are 1q41q44, 8q22q24, 19p12q13.1, 20q12q13, 3q26q29, 12p12p13, 2p22p25, 7p14p21, 5p15.2p15.3, and 17q22q25. The most common regions with loss of DNA copy numbers are Xp11.2q13, 4q31q35, Xp21p22.3, 18q22q23, 13q22q31, 9p22p24, and 16q22q24. High-level gains were detected at chromosomal regions of 1q41q44, 2p22p25, 3q26q29, and 19p12q13.1. Comparative analysis of primary and recurrent tumors showed that gains of 2p22p25, 19p12q13.1, and 20q12q13 and loss of 5q14q22 were more common in the recurrent high-grade tumors. About 85% of the tumors showed increases in DNA copy numbers in the regions (2p and 8q) harboring the myc family gene. Patients with tumor containing fewer than seven chromosomal aberrations showed longer survival time. CONCLUSION: The myc oncogene family may play a role in the pathogenesis of ovarian serous carcinomas. Our study suggests that tumors with gains of 2p22p25, 19p12q13.1, and 20q12q13 and loss of 5q14q22 may be at high risk for recurrence. Furthermore, the patients' survival time inversely correlates with the numbers of chromosomal alterations found in their tumors. CGH analysis may have a clinical application in predicting prognosis and risk of recurrence in patients with ovarian serous carcinomas.

Aged↗
PubMed2003

Current and future strategies for the treatment of malignant brain tumors.

Glioblastoma (GB) is the most common subtype of primary brain tumor in adults. These tumors are highly invasive, very aggressive, and often infiltrate critical neurological areas within the brain. The mean survival time after diagnosis of GB has remained unchanged during the last few decades, in spite of advances in surgical techniques, radiotherapy, and also chemotherapy; patients' survival ranges from 9 to 12 months after initial diagnosis. In the same time frame, with our increasing understanding and knowledge of the physiopathology of several cancers, meaningful advances have been made in the treatment and control of several cancers, such as breast, prostate, and hematopoietic malignancies. Although a number of the genetic lesions present in GB have been elucidated and our understanding of the progressions of this cancer has increased dramatically over the last few years, it has not yet been possible to harness this information towards developing effective cures. In this review, we will focus on the classical ways in which GB is currently being treated, and will introduce a novel therapeutic modality, i.e., gene therapy, which we believe will be used in combination with classical treatment strategies to prolong the life-span of patients and to ultimately be able to control and/or cure these brain tumors. We will discuss the use of several vector systems that are needed to introduce the therapeutic genes within either the tumor mass, if these are not resectable, or the tumor bed, after successful tumor resection. We also discuss different therapeutic modalities that could be exploited using gene therapy, i.e., conditional cytotoxic approach, direct cytotoxicity, immunotherapy, inhibition of angiogenesis, and the use of pro-apoptotic genes. The advantages and disadvantages of each of the current vector systems available to transfer genes into the CNS are also discussed. With the advances in molecular techniques, both towards the elucidation of the physiopathology of GB and the development of novel, more efficient and less toxic vectors to deliver putative therapeutic genes into the CNS, it should be possible to develop new rationale and effective therapeutic approaches to treat this devastating cancer.

Animals↗
PubMed2003

A Controllable and Observable Protein Cystallization Facility.

A Controllable and Observable Protein Crystallization Facility (ACOP) was developed in 1999 for space experiment in the Get Away Special canister of Space Shuttle. To regulate the vapor diffusion rate, in a crystallization chamber, five cells each containing precipitant solution of different concentrations, exposed to one protein cell in turn. Five layers of chambers were overlapped coaxially. The crystallization process was observed and recorded by digital cameras. Structure of facility and result of image sequence were given.

Crystallization↗
PubMed2003

Fourier-transform Raman and infrared spectroscopic analysis of 2-nitro-tetraphenylporphyrin and metallo-2-nitro-tetraphenylporphyrins.

The Fourier-transform Raman (FT-Raman) and infrared (FT-IR) spectra of 2-nitro-tetraphenylporphyrin (2-NO(2)-TPP), nickel-2-nitro-tetraphenylporphyrin (Ni-2-NO(2)-TPP), zinc-2-nitro-tetraphenylporphyrin (Zn-2-NO(2)-TPP) and copper-2-nitro-tetraphenylporphyrin (Cu-2-NO(2)-TPP) were acquired for the first time and carefully assigned and discussed. The effects of a beta-NO(2) group and the influence of the central metal on the molecular symmetry and vibrational spectra of the porphyrin macrocycle were also examined. The bands at 1323-1339, 1516-1526 and 961-971 cm(-1) were attributed to the symmetric and asymmetric stretching vibration of the NO(2) group and to the stretching vibration of the C(beta)-N bond, respectively, which connects the NO(2) group with the beta-carbon of the porphyrin macrocycle. These bands can act as a marker to distinguish beta-NO(2) TPPs from other beta-substituent TPPs. Cu-2-NO(2)-TPP has a C(4nu) molecular symmetry, which is different from those of Ni-2-NO(2)-TPP and Zn-2-NO(2)-TPP, i.e. D(4h).

Organometallic Compounds↗
PubMed2003

Response of Schwann cells in the inferior alveolar nerve to distraction osteogenesis: an ultrastructural and immunohistochemical study.

The biological mechanisms of nerve adaptation to distraction osteogenesis have not yet been elucidated. This study observed response of Schwann cells in the inferior alveolar nerve (IAN) following mandibular lengthening by electron microscopy and immunohistochemistry of S-100 protein, a specific marker of Schwann cells. Unilateral mandibular distraction (10mm elongation) was performed in nine young adult goats. Three animals were sacrificed at 7, 14 and 28 days after completion of distraction, respectively. The distracted IAN specimens and control nerves (from the contralateral sides) were harvested and processed for histological, ultrastructural and immunohistochemical examinations. Wallerian degeneration was observed in the distracted IAN, and Signs of axonal regeneration, as well as many activated Schwann cells were seen in the lengthened nerves. The expression of S-100 protein increased significantly at early stage of distraction osteogenesis, but almost returned to the normal level at 28 days after distraction. This study suggests that Wallerian degeneration caused by mechanical stretching may stimulate Schwann cells to enter a proliferated and activated state. Schwann cells and S-100 protein appear to play crucial roles in axonal regeneration that contributes to nerve adaptation to gradual distraction. Therefore, the IAN injury caused by mandibular gradual distraction was not serious; it seems to recover totally through a complicated repair mechanism.

Adaptation, Biological↗
PubMed2002

Analysis of origin and optimization of expansion and transduction of circulating peripheral blood endothelial progenitor cells in the rhesus macaque model.

Adult marrow-derived cells have been shown to contribute to various nonhematologic tissues and, conversely, primitive cells isolated from nonhematopoietic tissues have been shown to reconstitute hematopoiesis. Circulating endothelial progenitor cells (EPCs) have been reported to be at least partially donor derived after allogeneic bone marrow transplantation, and shown to contribute to neovascularization in murine ischemia models. However, it is unknown whether these EPCs are actually clonally derived from the same population of stem and progenitor cells that reconstitute hematopoiesis, or from another cell population found in the marrow or mobilized blood that is transferred during transplantation. To approach this question, we characterized circulating EPCs and also endothelial cells from large vessels harvested at autopsy from rhesus macaques previously transplanted with retrovirally transduced autologous CD34-enriched peripheral blood stem cells (PBSCs). Endothelial cells were grown in culture for 21-28 days and were characterized as CD31(+) CD14(-) via flow cytometry, as acLDL(+) UEA-1(+) via immunohistochemistry, and as Flk-1(+) by reverse transcriptase-polymerase chain reaction (RT-PCR). Animals had stable vector marking in hematopoietic lineages of 2-15%. Neither cultured circulating EPCs collected in steady state (n = 3), nor endothelial cells grown from large vessels (n = 2), had detectable retroviral marking. EPCs were CD34(+) and could be mobilized into the circulation with granulocyte colony-stimulating factor. Under ex vivo culture conditions, in which CD34(+) cells were optimized to transduce hematopoietic progenitor and stem cells, there was a marked depletion of EPCs. Transduction of EPCs was much more efficient under conditions supporting endothelial cell growth. Further elucidation of the origin and in vivo behavior of EPCs may be possible, using optimized transduction conditions and a vascular injury model.

3T3 Cells↗
PubMed2002

Alcohol, tobacco and breast cancer--collaborative reanalysis of individual data from 53 epidemiological studies, including 58,515 women with breast cancer and 95,067 women without the disease.

Alcohol and tobacco consumption are closely correlated and published results on their association with breast cancer have not always allowed adequately for confounding between these exposures. Over 80% of the relevant information worldwide on alcohol and tobacco consumption and breast cancer were collated, checked and analysed centrally. Analyses included 58,515 women with invasive breast cancer and 95,067 controls from 53 studies. Relative risks of breast cancer were estimated, after stratifying by study, age, parity and, where appropriate, women's age when their first child was born and consumption of alcohol and tobacco. The average consumption of alcohol reported by controls from developed countries was 6.0 g per day, i.e. about half a unit/drink of alcohol per day, and was greater in ever-smokers than never-smokers, (8.4 g per day and 5.0 g per day, respectively). Compared with women who reported drinking no alcohol, the relative risk of breast cancer was 1.32 (1.19-1.45, P<0.00001) for an intake of 35-44 g per day alcohol, and 1.46 (1.33-1.61, P<0.00001) for >/=45 g per day alcohol. The relative risk of breast cancer increased by 7.1% (95% CI 5.5-8.7%; P<0.00001) for each additional 10 g per day intake of alcohol, i.e. for each extra unit or drink of alcohol consumed on a daily basis. This increase was the same in ever-smokers and never-smokers (7.1% per 10 g per day, P<0.00001, in each group). By contrast, the relationship between smoking and breast cancer was substantially confounded by the effect of alcohol. When analyses were restricted to 22 255 women with breast cancer and 40 832 controls who reported drinking no alcohol, smoking was not associated with breast cancer (compared to never-smokers, relative risk for ever-smokers=1.03, 95% CI 0.98-1.07, and for current smokers=0.99, 0.92-1.05). The results for alcohol and for tobacco did not vary substantially across studies, study designs, or according to 15 personal characteristics of the women; nor were the findings materially confounded by any of these factors. If the observed relationship for alcohol is causal, these results suggest that about 4% of the breast cancers in developed countries are attributable to alcohol. In developing countries, where alcohol consumption among controls averaged only 0.4 g per day, alcohol would have a negligible effect on the incidence of breast cancer. In conclusion, smoking has little or no independent effect on the risk of developing breast cancer; the effect of alcohol on breast cancer needs to be interpreted in the context of its beneficial effects, in moderation, on cardiovascular disease and its harmful effects on cirrhosis and cancers of the mouth, larynx, oesophagus and liver.

Adult↗
PubMed2002

Tetrasomy 15q25.3 --> qter resulting from an analphoid supernumerary marker chromosome in a patient with multiple anomalies and bilateral Wilms tumors.

We describe a girl who had been followed since birth for apparent Shprintzen-Goldberg syndrome (SGS), with macrosomia, long fingers and toes, and craniosynostosis, and presented at 4 years of age with bilateral Wilms tumors (also called nephroblastoma). Cytogenetic analysis of her peripheral blood revealed a de novo supernumerary marker chromosome. This stable marker chromosome is present in 19 of 20 lymphocytes analyzed, as well as in all 40 tumor cells (20 from each tumor) studied. Classical and molecular cytogenetic studies indicate that the marker is derived from an inverted duplication of chromosome 15q25.3 --> qter and contains a neocentromere. The presence of this marker chromosome in our patient results in tetrasomy 15q25.3 --> qter. The relationship between her genotype and phenotype are discussed in light of genes, including IGF1R and FES, mapped to the aneusomic segment.

Abnormalities, Multiple↗
PubMed2002

High-resolution genome-wide allelotype analysis identifies loss of chromosome 14q as a recurrent genetic alteration in astrocytic tumours.

Diffusely infiltrative astrocytic tumours are the most common neoplasms in the human brain. To localise putative tumour suppressor loci that are involved in low-grade astrocytomas, we performed high-resolution genome-wide allelotype analysis on 17 fibrillary astrocytomas. Non-random allelic losses were identified on chromosomal arms 10p (29%), 10q (29%), 14q (35%), 17p (53%), and 19q (29%), with their respective common regions of deletions delineated at 10p14-15.1, 10q25.1-qter, 14q212.2-qer, 17p11.2-pter and 19q12-13.4. These results suggest that alterations of these chromosomal regions play important roles in the development of astrocytoma. We also allelotyped 21 de novo glioblastoma multiforme with an aim to unveil genetic changes that are common to both types of astrocytic tumours. Non-random allelic losses were identified on 9p (67%), 10p (62%), 10q (76%), 13q (60%), 14q (50%), and 17p (65%). Allelic losses of 10p, 10q, 14q and 17p were common genetic alterations detectable in both fibrillary astrocytomas and glioblastoma multiforme. In addition, two common regions of deletions on chromosome 14 were mapped to 14q22.3-32.1 and 14q32.1-qter, suggesting the presence of two putative tumour suppressor genes. In conclusion, our comprehensive allelotype analysis has unveiled several critical tumour suppressor loci that are involved in the development of fibrillary astrocytomas and glioblastoma multiforme. Although these two types of brain tumours are believed to evolve from different genetic pathways, they do share some common genetic changes. Our results indicate that deletions of chromosome 14q is a recurrent genetic event in the development of astrocytoma and highlight the subchromosomal regions on this chromosome that are likely to contain putative tumour suppressor genes involved in the oncogenesis of astrocytic tumours.

Adult↗
PubMed2002

A CD200FC immunoadhesin prolongs rat islet xenograft survival in mice.

BACKGROUND: A solubilized form of the CD200 molecule, CD200Fc, has been shown to suppress allograft rejection and development of collagen-induced arthritis in mice. We investigated whether the same molecule could prolong survival of rat islet xenografts. METHODS: Streptozocin-treated mice, receiving injections with anti-asialo-GM1 antibody, received rat islets ( approximately 400/mouse) under the kidney capsule or injected into the portal vein, along with rapamycin treatment. Thereafter mice received injections of CD200Fc (10 microg/mouse/injection) or control mouse IgG2. Blood glucose was monitored daily. Some mice received additional injections of anti-CD200/-CD200R monoclonal antibodies. RESULTS: Portal vein delivery of islets led to more extended resolution of diabetes than did transplantation under the kidney capsule. CD200Fc further prolonged survival in either case, an effect abolished by anti-CD200 or F(ab')2 anti-CD200R mAbs, but not by whole anti-CD200R (anti-CD200R Ig). Spleen cells taken from CD200Fc-treated mice showed polarization to type-2 cytokine production (interleukin-4, interleukin-10) on restimulation with rat splenocytes in culture, in comparison to cells from control mice (type-1 cytokines, interlulin-2, interferon-gamma). CONCLUSION: CD200:CD200R interactions are important in regulating rat islet xenograft survival.

Animals↗
PubMed2002

First measurement of the double spin asymmetry in (-->)e(-->)p-->e(prime)pi(+)n in the resonance region.

The double spin asymmetry in the (-->)e(-->)p --> e(prime)pi(+)n reaction has been measured for the first time in the resonance region for four-momentum transfer Q2 = 0.35-1.5 GeV(2). Data were taken at Jefferson Lab with the CLAS detector using a 2.6 GeV polarized electron beam incident on a polarized solid NH3 target. Comparison with predictions of phenomenological models shows strong sensitivity to resonance contributions. Helicity-1/2 transitions are found to be dominant in the second and third resonance regions. The measured asymmetry is consistent with a faster rise with Q(2) of the helicity asymmetry A1 for the F(15)(1680) resonance than expected from the analysis of the unpolarized data.

Journal Article↗
PubMed2002

Vascular phenotype in angiogenic and non-angiogenic lung non-small cell carcinomas.

We have previously described a group of non-small cell lung carcinomas without morphological evidence of neo-angiogenesis. In these tumours neoplastic cells fill up the alveoli and the only vessels present appear to belong to the trapped alveolar septa. In the present study we have characterised the phenotype of the vessels present in these non-angiogenic tumours, in normal lung and in angiogenic non-small cell lung carcinomas. The vessels, identified by the expression of CD31, were scored as mature when expressing the epitope LH39 in the basal membrane and as newly formed when expressing alphaVbeta3 on the endothelial cells and/or lacking LH39 expression. In the nine putative non-angiogenic cases examined, the vascular phenotype of all the vessels was the same as that of alveolar vessels in normal lung: LH39 positive and alphaVbeta3 variable or negative. Instead in 104 angiogenic tumours examined, only a minority of vessels (mean 13.1%; range 0--60%) expressed LH39, while alphaVbeta3 (in 45 cases) was strongly expressed on many vessels (mean 55.5%; range 5--90%). We conclude that in putative non-angiogenic tumours the vascular phenotype is that of normal vessels and there is no neo-angiogenesis. This type of cancer may be resistant to some anti-angiogenic therapy and different strategies need to be developed.

Carcinoma, Non-Small-Cell Lung↗
PubMed2002

Further evidence for the decay K+ -->pi+nu(nu).

Additional evidence for the rare kaon decay K+-->pi+nu(nu) has been found in a new data set with comparable sensitivity to the previously reported result. One new event was observed in the pion momentum region examined, 211 pi+nu(nu)) = 1.57(+1.75)(-0.82)x10(-10).

Journal Article↗
PubMed2002

Canadian male farm residents, pesticide safety handling practices, exposure to animals and non-Hodgkin's lymphoma (NHL).

BACKGROUND: A majority of published studies indicate that farmers have an elevated risk of developing non-Hodgkin's lymphoma (NHL) compared to other workers. METHODS: We evaluated accidental exposure to pesticides, the use of personal protective equipment, and exposure to animals among male farm residents in a Canadian population-based, multi-centre, NHL-control questionnaire study. RESULTS: In a multivariate model, the following variables had statistically significant adjusted odds ratios (OR) using 95% confidence intervals (95% CI) (a) higher risk: having more than 13 head of swine, raising bison, elk or ostriches, a personal history of cancer, > 4 and < or = 15 years of farm residence and occupational exposure to diesel fuel and exhaust; (b) lower risk: raising cattle and a personal history of measles. CONCLUSIONS: Future multidisciplinary studies of NHL should include a comprehensive review of exposure to animals in sufficient detail to assess etiological mechanisms to explain the putative associations between exposure to farm animals and NHL.

Adult↗