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Biomedical subjects

Y Ji

Publications and source records attributed to Y Ji.

At least 55 records · Page 3Linked to original sources
PubMed2001

Hepatic angiomyolipoma: a clinicopathologic study of 10 cases.

OBJECTIVE: To study the clinicopathologic features of hepatic angiomyolipoma (AML) and to investigate the feasibility of a new antibody-A103 as a diagnostic aid for AML. METHODS: Ten cases of AML were retrieved from hospital records and analyzed morphologically. Immunohistochemistry was performed on paraffin-embedded tissues with a panel of antibodies, including antibody-A103. RESULTS: There were eight women and two men, with ages ranging from 38-58 years (median 45.7). Clinically, nine cases were asymptomatic and found by imaging techniques. None of the patients had associated tuberous sclerosis. All tumors were sharply demarcated from the surrounding liver parenchyma. Histologically they were composed of a heterogeneous mixture of three components: thick-walled blood vessels, spindle or epithelioid smooth muscle cells and adipose tissue. All tumors showed a strong immunoreactivity to A103, HMB-45 and smooth muscle actins. Follow-up information on all 10 cases showed a benign course with no signs of recurrence. CONCLUSIONS: Hepatic AML is a rare mesenchymal tumor of the liver. A103 is a promising marker for a pathologic diagnosis of hepatic AML.

Actins↗
PubMed2001

Peri-operative treatment of most severely head-injured patients.

OBJECTIVE: To summarize the peri-operative experience from 53 patients with traumatic head injuries with GCS score 3-5. METHODS: Fifty-three most severely head-injured patients with GCS score 3-5 were admitted to our department and treated operatively from Oct. 1994 to Jun. 1998 and the data were analyzed retrospectively. RESULTS: Thirty-seven cases (69.8%) survived, among them 28 (52.8%) had a good recovery or moderate disability, and 9 (17%) had severe deficits. The other 16 (30.2%) died after therapy. CONCLUSIONS: The prognosis of most severely head-injured patients could be improved by peri-operative treatment including premedical care, early evacuation of intracranial hematoma with large decompressive craniectomies, intracranial hypertension monitoring, moderate hypothermia therapy, effective prevention and treatment of cerebral vasospasm and complications.

Adolescent↗
PubMed2001

Clinical analysis on 149 old patients with craniocerebral injury.

OBJECTIVE: To study the clinical features of craniocerebral injury (CI) in the aged. METHODS: The data of 149 old patients with CI hospitalized in t he department from July 1991 to May 2000 were studied retrospectively in this study. The causes of injury, traumatic pathology, clinical manifestation and cause s of death were analyzed, too. RESULTS: Automobiles were the main victim-makers, and falls we re the second. And there was no significant difference between the first two kin ds of victim-makers. The patients suffered mainly from cerebral contusion, intracerebral hematomas and subdural hematomas, and relatively fewer from epidural hematomas. The scores of Glasgow Coma Scale (GCS) were related closely to the prognosis when hospitalized or before surgical treatment. The total mortality rate was 37.5% in this study. The main cause of death was brain injury. CONCLUSIONS: The old patients with CI have a high mortality rat e. And the causes of injury, traumatic pathology and clinical manifestation are peculiar in the aged.

Aged↗
PubMed2001

[The significance of thrombosis after experimental pulmonary thromboembolism].

OBJECTIVE: To study the significance of thrombosis after experimental pulmonary thromboembolism (PTE). METHODS: Acute PTE models of rabbits were established with injection of autologous blood clots (0.04 g/kg) stabilized in a temperature-controlled (70 degrees C) of distilled water for 10 minutes through the femoral vein, then the regulation of thrombosis was explored at dissection and upon microscopic examination after PTE. Moreover, the coagulability of blood and the plasma level of thromboxane A2(TXA2) and endothelin (ET) were examined. RESULTS: Thrombotic propensity was found at 1 h, and fresh thrombosis started to form at 24 h following clots infusion. Emboli were completely or partly dissolved at 5 d and organized at 10 and 14 d after clots infused. Prothrombin time was significantly lower [(7.15 +/- 0.06)s], and fibrinogen was higher [(5.86 +/- 1.50) g/L] at 24 h post-clots, compared with pre-clots [(7.34 +/- 0.19)s, (3.37 +/- 1.02) g/L] (P < 0.05). Venous plasma level of TXA2 began to increase at 5 min [(2.5 +/- 0.7) micrograms/L] and continued to rise to its maximum at 15 min [(2.5 +/- 0.6) micrograms/L], then declined at 60 min after clots infusion. The level of ET in both arterial and venous blood increased at 5 d post-clots [(0.84 +/- 0.15) micrograms/L and (0.23 +/- 0.05) micrograms/L] separately, while most of emboli resolved. CONCLUSIONS: There is thrombus formation after autologous-blood-clots-induced PTE. Furthermore, thrombus formation, fibrinolysis and organization may always interact on each other consistently, and control the pathogenesis of PTE. Abnormalities of ET metabolism occur after PTE and the major mediator of TXA2 plays an important role in the early phase of PTE.

Animals↗
PubMed2001

[The alternative splicing & expression of fibronectin IIIcs segment and its relationship with wound healing].

Fibronectin is an important large adhesive glycoprotein of the extracellular matrix, which is alternatively spliced in three regions, designated EIIIA, EIIIB and IIIcs respectively. IIIcs contains two binding domains for a variety of cell surface and extracellular ligands. Through this multiplicity of adhesive activities, IIIcs can fulfill key roles in a broad spectrum of physiological processes, such as cell spreading and migration, differentiation and embryogenesis, wound healing, malignant transformation and metastasis, etc. Here, we will discuss the structure, biological property, and function of IIIcs splicing variants and its forensic applications.

Alternative Splicing↗
PubMed2000

Disruption of a single copy of the SERCA2 gene results in altered Ca2+ homeostasis and cardiomyocyte function.

A mouse model carrying a null mutation in one copy of the sarcoplasmic reticulum (SR) Ca(2+)-ATPase isoform 2 (SERCA2) gene, in which SERCA2 protein levels are reduced by approximately 35%, was used to investigate the effects of decreased SERCA2 level on intracellular Ca(2+) homeostasis and contractile properties in isolated cardiomyocytes. When compared with wild-type controls, SR Ca(2+) stores and Ca(2+) release in myocytes of SERCA2 heterozygous mice were decreased by approximately 40-60% and approximately 30-40%, respectively, and the rate of myocyte shortening and relengthening were each decreased by approximately 40%. However, the rate of Ca(2+) transient decline (tau) was not altered significantly, suggesting that compensation was occurring in the removal of Ca(2+) from the cytosol. Phospholamban, which inhibits SERCA2, was decreased by approximately 40% in heterozygous hearts, and basal phosphorylation of Ser-16 and Thr-17, which relieves the inhibition, was increased approximately 2- and 2.1-fold. These results indicate that reduced expression and increased phosphorylation of phospholamban provides compensation for decreased SERCA2 protein levels in heterozygous heart. Furthermore, both expression and current density of the sarcolemmal Na(+)-Ca(2+) exchanger were up-regulated. These results demonstrate that a decrease in SERCA2 levels can directly modify intracellular Ca(2+) homeostasis and myocyte contractility. However, the resulting deficit is partially compensated by alterations in phospholamban/SERCA2 interactions and by up-regulation of the Na(+)-Ca(2+) exchanger.

Animals↗
PubMed2000

Solution structure of BmP02, a new potassium channel blocker from the venom of the Chinese scorpion Buthus martensi Karsch.

BmP02 is a 28-amino acid residue peptide purified from the venom of the Chinese scorpion Buthus martensi Karsch, which had been demonstrated to be a weak blocker of apamin-sensitive calcium-activated potassium channels. Two-dimensional NMR spectroscopy techniques were used to determine the solution structure of BmP02. The results show that BmP02 formed a alpha/beta scorpion fold, the typical three-dimensional structure adopted by most short chain scorpion toxins whose structures have been determined. However, in BmP02 this alpha/beta fold was largely distorted. The alpha-helix was shortened to only one turn, and the loop connecting the helix to the first beta-strand exhibited conformational heterogeneity. The instability of BmP02 could be attributed to a proline at position 17, which is usually a glycine. Because the residue at this position makes intense contact with the alpha-helix, it was supposed that the bulky side chain of proline had pushed the helix away from the beta-sheet. This had a significant influence on the structure and function of BmP02. The alpha-helix rotated by about 40 degrees to avoid Pro17 while forming two disulfides with the second beta-strand. The rotation further caused both ends of the helix to be unwound due to covalent restrictions. According to its structure, BmP02 was supposed to interact with its target via the side chains of Lys11 and Lys13.

Amino Acid Sequence↗
PubMed2000

Phase evolution in a Kondo-correlated system.

We measured the phase evolution of electrons as they traverse a quantum dot (QD) formed in a two-dimensional electron gas that serves as a localized spin. The traversal phase, determined by embedding the QD in a double path electron interferometer and measuring the quantum interference of the electron wave functions manifested by conductance oscillation as a function of a weak magnetic field, evolved by pi radians, a range twice as large as theoretically predicted. As the correlation weakened, a gradual transition to the familiar phase evolution of a QD was observed. The specific phase evolution observed is highly sensitive to the onset of Kondo correlation, possibly serving as an alternative fingerprint of the Kondo effect.

Journal Article↗
PubMed2000

Isolation and molecular characterization of the 5'-upstream region of the human TRAIL gene.

TRAIL, a novel member of the TNF family, acts through membrane receptors to induce apoptosis of activated T lymphocytes and may represent a mechanism for the "immune escape" of certain cancers. Various cytokines appear to increase expression of other TNF family members; however, the regulation of TRAIL has not been defined. The purpose of this study was to assess molecular mechanisms regulating TRAIL gene expression in human colon cancers. In this study, we have cloned the human TRAIL (hTRAIL) promoter ( approximately 1.6 kb) and identified a number of putative transcription factor binding sites such as NFAT, AP-1 and Sp1 sequences which are important for the expression of other TNF family members. Transient transfections of 5'-deletion promoter constructs into either Caco-2 or HT29 colon cancer cells identified TRAIL promoter regions critical for both basal and interferon-gamma (IFN-gamma)-mediated induction. Furthermore, induction of TRAIL mRNA levels was demonstrated in HT29 and Caco-2 cells with IFN-gamma treatment suggesting an important role for this cytokine in TRAIL expression.

Apoptosis Regulatory Proteins↗
PubMed2000

Overexpression of SERCA2b in the heart leads to an increase in sarcoplasmic reticulum calcium transport function and increased cardiac contractility.

The sarcoplasmic reticulum calcium ATPase SERCA2b is an alternate isoform encoded by the SERCA2 gene. SERCA2b is expressed ubiquitously and has a higher Ca(2+) affinity compared with SERCA2a. We made transgenic mice that overexpress the rat SERCA2b cDNA in the heart. SERCA2b mRNA level was approximately approximately 20-fold higher than endogenous SERCA2b mRNA in transgenic hearts. SERCA2b protein was increased 8-10-fold in the heart, whereas SERCA2a mRNA/protein level remained unchanged. Confocal microscopy showed that SERCA2b is localized preferentially around the T-tubules of the SR, whereas SERCA2a isoform is distributed both transversely and longitudinally in the SR membrane. Calcium-dependent calcium uptake measurements showed that the maximal velocity of Ca(2+) uptake was not changed, but the apparent pump affinity for Ca(2+) (K(0.5)) was increased in SERCA2b transgenic mice (0.199 +/- 0.011 micrometer) compared with wild-type control mice (0.269 +/- 0.012 micrometer, p < 0.01). Work-performing heart preparations showed that SERCA2b transgenic hearts had a higher rates of contraction and relaxation, shorter time to peak pressure and half-time for relaxation than wild-type hearts. These data show that SERCA2b is associated in a subcompartment within the sarcoplasmic reticulum of cardiac myocytes. Overexpression of SERCA2b leads to an increase in SR calcium transport function and increased cardiac contractility, suggesting that SERCA2b plays a highly specialized role in regulating the beat-to-beat contraction of the heart.

Animals↗
PubMed2000

Effects of cholinergic agents on spontaneous activity of nucleus basalis magnocellularis neurons in different age rats.

The present study investigated the effects of intracerebroventricular (i.c.v.) injection of acetylcholine (Ach), atropine and tubocurarine on the spontaneous activity of nucleus basalis Magnocellularis (nbM) neurons in young, adult and old rats. I.c.v. injection of Ach (1, 10 and 100 mM) dose-dependently increased the spontaneous firing rate in most of the nbM neurons (66.7%). The Ach-induced excitation effect on the spontaneous firing of nbM neurons was decreased with aging. I.c.v. injection of atropine (2.5, 25 and 250 mM) or tubocurarine (0.1, 1 and 10 mM) not only antagonized the Ach-induced excitation, but also inhibited the spontaneous firing of nbM neurons. The inhibitory effects were gradually decreased with aging. These results suggested that there might be some functional changes in nbM neurons with aging, which impair their responsive ability to stimuli of drugs.

Acetylcholine↗
PubMed2000

Nucleotide sequence analyses of partial envgp46 gene of human T-lymphotropic virus type I from inhabitants of Fujian Province in Southeast China.

Partial sequences from the env(gp46) gene of two human T-lymphotropic virus type I (HTLV-I) isolates (LIN and WEN) obtained from inhabitants of Fujian Province in southeast China were analyzed. A phylogenetic tree was constructed from these sequence data and those of other known HTLV-I isolates from all over the world. Comparisons of the LIN and WEN nucleotide sequences with other HTLV-I isolates showed diversity ranging from 0.73 to 7.00% for LIN and from 0.87 to 7.00% for WEN. Sequences of isolates LIN, WEN, MT-2, TSP1, and CH were most closely related, and the phylogenetic tree showed that all belong to the widespread subtype A of the cosmopolitan group. These preliminary data indicate that HTLV-I isolates from Fujian Province, China are closely related to HTLV-I strains from Japan and the Caribbean.

Base Sequence↗
PubMed2000

The expression of SR calcium transport ATPase and the Na(+)/Ca(2+)Exchanger are antithetically regulated during mouse cardiac development and in Hypo/hyperthyroidism.

The mouse has been used extensively for generating transgenic animal models to study cardiovascular disease. Recently, a number of transgenic mouse models have been created to investigate the importance of sarcoplasmic reticulum (SR) Ca(2+)transport proteins in cardiac pathophysiology. However, the expression and regulation of cardiac SR Ca(2+)ATPase and other Ca(2+)transport proteins have not been studied in detail in the mouse. In this study, we used multiplex RNase mapping analysis to determine SERCA2, phospholamban (PLB), and Na(+)/Ca(2+)-exchanger (NCX-1) gene expression throughout mouse heart development and in hypo/hyperthyroid animals. Our results demonstrate that the expression of SERCA2 and PLB mRNA increase eight-fold from fetal to adult stages, indicating that SR function increases with heart development. In contrast, the expression of the Na(+)/Ca(2+)-exchanger gene is two-fold higher in fetal heart compared to adult. Our study also makes the important observation that in hypothyroidic hearts the NCX-1 mRNA and protein levels were upregulated, whereas the SERCA2 mRNA/protein levels were downregulated. In hyperthyroidic hearts, however, an opposite response was identified. These findings are important and point out that the expression of NCX-1 is regulated antithetically to that of SERCA2 during heart development and in response to alterations in thyroid hormone levels.

Animals↗
PubMed2000

Structure of the highly conserved HERC2 gene and of multiple partially duplicated paralogs in human.

Recombination between chromosome-specific low-copy repeats (duplicons) is an underlying mechanism for several genetic disorders. Recently, a chromosome 15 duplicon was discovered in the common breakpoint regions of Prader-Willi and Angelman syndrome deletions. We identified previously the large HERC2 transcript as an ancestral gene in this duplicon, with approximately 11 HERC2-containing duplicons, and demonstrated that recessive mutations in mouse Herc2 lead to a developmental syndrome, juvenile development and fertility 2 (jdf2). We have now constructed and sequenced a genomic contig of HERC2, revealing a total of 93 exons spanning approximately 250 kb and a CpG island promoter. A processed ribosomal protein L41 pseudogene occurs in intron 2 of HERC2, and putative VNTRs occur in intron 70 (28 copies, approximately 76-bp repeat) and 3' exon 40 through intron 40 (6 copies, approximately 62-bp repeat). Sequence comparisons show that HERC2-containing duplicons have undergone several deletion, inversion, and dispersion events to form complex duplicons in 15q11, 15q13, and 16p11. To further understand the developmental role of HERC2, a highly conserved Drosophila ortholog was characterized, with 70% amino acid sequence identity to human HERC2 over the carboxy-terminal 743 residues. Combined, these studies provide significant insights into the structure of complex duplicons and into the evolutionary pathways of formation, dispersal, and genomic instability of duplicons. Our results establish that some genes not only have a protein coding function but can also play a structural role in the genome.

Amino Acid Sequence↗
PubMed2000

Structure of chromosomal duplicons and their role in mediating human genomic disorders.

Chromosome-specific low-copy repeats, or duplicons, occur in multiple regions of the human genome. Homologous recombination between different duplicon copies leads to chromosomal rearrangements, such as deletions, duplications, inversions, and inverted duplications, depending on the orientation of the recombining duplicons. When such rearrangements cause dosage imbalance of a developmentally important gene(s), genetic diseases now termed genomic disorders result, at a frequency of 0.7-1/1000 births. Duplicons can have simple or very complex structures, with variation in copy number from 2 to >10 repeats, and each varying in size from a few kilobases in length to hundreds of kilobases. Analysis of the different duplicons involved in human genomic disorders identifies features that may predispose to recombination, including large size and high sequence identity between the recombining copies, putative recombination promoting features, and the presence of multiple genes/pseudogenes that may include genes expressed in germ cells. Most of the chromosome rearrangements involve duplicons near pericentromeric regions, which may relate to the propensity of such regions to accumulate duplicons. Detailed analyses of the structure, polymorphic variation, and mechanisms of recombination in genomic disorders, as well as the evolutionary origin of various duplicons will further our understanding of the structure, function, and fluidity of the human genome.

Animals↗
PubMed2000

Infection of human dendritic cells by a sindbis virus replicon vector is determined by a single amino acid substitution in the E2 glycoprotein.

The ability to target antigen-presenting cells with vectors encoding desired antigens holds the promise of potent prophylactic and therapeutic vaccines for infectious diseases and cancer. Toward this goal, we derived variants of the prototype alphavirus, Sindbis virus (SIN), with differential abilities to infect human dendritic cells. Cloning and sequencing of the SIN variant genomes revealed that the genetic determinant for human dendritic cell (DC) tropism mapped to a single amino acid substitution at residue 160 of the envelope glycoprotein E2. Packaging of SIN replicon vectors with the E2 glycoprotein from a DC-tropic variant conferred a similar ability to efficiently infect immature human DC, whereupon those DC were observed to undergo rapid activation and maturation. The SIN replicon particles infected skin-resident mouse DC in vivo, which subsequently migrated to the draining lymph nodes and upregulated cell surface expression of major histocompatibility complex and costimulatory molecules. Furthermore, SIN replicon particles encoding human immunodeficiency virus type 1 p55(Gag) elicited robust Gag-specific T-cell responses in vitro and in vivo, demonstrating that infected DC maintained their ability to process and present replicon-encoded antigen. Interestingly, human and mouse DC were differentially infected by selected SIN variants, suggesting differences in receptor expression between human and murine DC. Taken together, these data illustrate the tremendous potential of using a directed approach in generating alphavirus vaccine vectors that target and activate antigen-presenting cells, resulting in robust antigen-specific immune responses.

Adenovirus E2 Proteins↗
PubMed2000

Alphavirus DNA and particle replicons for vaccines and gene therapy.

Alphaviruses have several features that make them attractive as gene delivery platforms, and vectors derived principally from Sindbis virus (SIN), Semliki Forest virus (SFV), and Venezuelan equine encephalitis virus (VEE), are currently being developed as prophylactic and therapeutic vaccines for infectious diseases and cancer. Alphavirus vectors, termed "replicons", retain the nonstructural protein genes encoding the viral replicase, that in turn programme high level cytoplasmic amplification of the vector RNA. We have developed plasmid DNA and recombinant vector particle delivery systems derived from the prototype alphavirus, SIN. Each system uses RNA polymerase II-based expression of alphavirus genome components and both vector formats are highly efficacious towards inducing robust antigen-specific immune responses in vaccinated animals. To increase the potency of SIN vector particles, which are not known to be lymphotropic, the tropism was re-directed for efficient infection of dendritic cells, both in vitro and in vivo.

Alphavirus↗