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Biomedical subjects

T Chi

Publications and source records attributed to T Chi.

At least 19 recordsLinked to original sources
PubMed1999

Spectro-temporal modulation transfer functions and speech intelligibility.

Detection thresholds for spectral and temporal modulations are measured using broadband spectra with sinusoidally rippled profiles that drift up or down the log-frequency axis at constant velocities. Spectro-temporal modulation transfer functions (MTFs) are derived as a function of ripple peak density (omega cycles/octave) and drifting velocity (omega Hz). The MTFs exhibit a low-pass function with respect to both dimensions, with 50% bandwidths of about 16 Hz and 2 cycles/octave. The data replicate (as special cases) previously measured purely temporal MTFs (omega = 0) [Viemeister, J. Acoust. Soc. Am. 66, 1364-1380 (1979)] and purely spectral MTFs (omega = 0) [Green, in Auditory Frequency Selectivity (Plenum, Cambridge, 1986), pp. 351-359]. A computational auditory model is presented that exhibits spectro-temporal MTFs consistent with the salient trends in the data. The model is used to demonstrate the potential relevance of these MTFs to the assessment of speech intelligibility in noise and reverberant conditions.

Auditory Threshold↗
PubMed1999

Iatrogenic abdominal scar endometriosis: a case report.

We report the case of a patient with abdominal scar endometriosis following a cesarean section. The rarity of this localization and its appearance on computerized tomography is shown. We emphasize the combination of history and image study of this pathology in the differential diagnosis of other diseases.

Abdominal Muscles↗
PubMed1998

Defects in actin-cap formation in Vav-deficient mice implicate an actin requirement for lymphocyte signal transduction.

BACKGROUND: Antigen-receptor interactions on lymphocytes result in local clustering of actin, receptors and signaling molecules into an asymmetric membrane structure termed a cap. Although actin polymerization is known to be required, the mechanisms underlying cap formation are unclear. We have studied the events underlying cap formation using mice bearing a null mutation in vav (vav-/-), a gene that encodes a guanine-nucleotide exchange factor for the GTPase Rac. RESULTS: Lymphocytes from vav-/- mice failed to form T-cell receptor caps following activation and had a defective actin cytoskeleton. The vav-/- T cells were deficient in interleukin-2 (IL-2) production and proliferation, and the peak of Ca2+ mobilization was reduced although of normal duration. Activation of Jun N-terminal kinase or stress-activated kinase (JNK or SAPK) and mitogen-activated protein kinase (MAPK) and the induction of the transcription factor NF-ATc1 and egr-1 genes was normal. Despite the reduced Ca2+ mobilization, translocation of cytoplasmic NF-ATc to the nucleus was normal, reflecting that the lower levels of Ca2+ in vav-/- cells were still sufficient to activate calcineurin. Treatment of lymphocytes with cytochalasin D, which blocks actin polymerization, inhibited cap formation and produced defects in signaling and IL-2 transcriptional induction in response to antigen-receptor signaling that were nearly identical to those seen in vav-/- cells. In transfection studies, either constitutively active Vav or Rac could complement constitutively active calcineurin to activate NF-AT-dependent transcription. CONCLUSIONS: These results indicate that Vav is required for cap formation in lymphocytes. Furthermore, the correlation between cap formation, IL-2 production and proliferation supports the hypothesis that an actin-dependent pathway is a source of specialized growth regulatory signals.

Actins↗
PubMed1998

Architectural DNA binding by a high-mobility-group/kinesin-like subunit in mammalian SWI/SNF-related complexes.

The SWI/SNF complex in yeast and Drosophila is thought to facilitate transcriptional activation of specific genes by antagonizing chromatin-mediated transcriptional repression. The mechanism by which it is targeted to specific genes is poorly understood and may involve direct DNA binding and/or interactions with specific or general transcription factors. We have previously purified a mammalian complex by using antibodies against BRG1, a human homologue of SWI2/SNF2. This complex is likely functionally related to the yeast SWI/SNF complex because all five subunit identified so far (referred to as BAFs, for BRG1-associated factors) are homologues of the yeast SWI/SNF subunits. However, we now describe the cloning of the 57-kDa subunit (BAF57), which is present only in higher eukaryotes but not in yeast. BAF57 is shared by all mammalian complexes and contains a high-mobility-group (HMG) domain adjacent to a kinesin-like region. Both recombinant BAF57 and the whole complex bind four-way junction (4WJ) DNA, which is thought to mimic the topology of DNA as it enters or exits the nucleosome. Surprisingly, complexes with mutations in the HMG domain of BAF57 can still bind 4WJ DNA and mediate ATP-dependent nucleosome disruption. Our work describes the first DNA binding subunit for SWI/SNF-like complexes and suggest that the mechanism by which mammalian and Drosophila SWI/SNF-like complexes interact with chromatin may involve recognition of higher-order chromatin structure by two or more DNA binding domains.

Amino Acid Sequence↗
PubMed1998

Delayed intestinal stenosis after blunt abdominal trauma: report of a case.

Major intestinal injury may be present with very subtle clinical and/or imaging findings. Sometimes, delayed intestinal stenosis may occur even several months after the blunt abdominal trauma. We present a 12-year-old boy with delayed jejunal stenosis following blunt abdominal injury in a car collision. Computed tomography (CT) scan showed streaky infiltrates in the mesentery and fluid densities in the bilateral anterior pararenal spaces as well as enhancement of bowel wall on the 2nd day after trauma. A "bird-beak" sign at the proximal jejunum with diffuse mucosal swelling of jejunal loops were seen on barium follow-up study on the 7th day. Complete obstruction at the duodenojejunal junction was identified by the follow-up barium examination on the 29th day.

Abdominal Injuries↗
PubMed1996

Assembly of the isomerized TFIIA--TFIID--TATA ternary complex is necessary and sufficient for gene activation.

The prevailing view of eukaryotic gene activation poses that activators stimulate transcription by recruiting limiting components of the general transcription machinery to a core promoter. In one such model case, activation by the Epstein-Barr virus ZEBRA protein correlated closely with recruitment of the general transcription factors TFIIA and TFIID (the DA complex) as measured by DNase I footprinting and gel mobility shift assays. We now report that simple recruitment is not sufficient for full-level activation. An additional concentration-independent, rate-limiting step is activator-mediated isomerization of the DA complex characterized by an extended TFIID footprint. The isomerized complex supports both binding of TFIIB in gel mobility shift assays and activated transcription in heat-treated nuclear extracts, even after removal of ZEBRA. Surprisingly, the regulatory phenomenon of synergy was manifested only when the concentration of TFIID was limiting. When the DA complex was saturating, transcription was not synergistic, as indicated by the ability of a single activator to induce isomerization effectively and turn on a gene. On the basis of these observations, we propose a new biochemical model for eukaryotic gene activation and synergy.

DNA-Binding Proteins↗
PubMed1996

Healing of chondral and osteochondral defects in a canine model: the role of cultured chondrocytes in regeneration of articular cartilage.

In this study a canine model was developed to investigate the nature of early healing responses to both chondral and osteochondral defects and to evaluate the tissue regenerative capacity of cultured autologous chondrocytes in chondral defects. The healing response to surgically created chondral defects was minor, with little cellular infiltration. In contrast, osteochondral defects exhibited a rapid cellular response, resulting ultimately in the formation of fibrous tissue. The lack of significant cellular activity in chondral defects suggests that an evaluation of the capacity of cultured autologous chondrocytes to regenerate articular cartilage is best studied in chondral defects using the canine model. When dedifferentiated cultured articular chondrocytes were implanted into chondral defects, islands of type II collagen staining were demonstrated in the regenerative tissue within 6 weeks. The relatively early expression of cartilage specific markers by the implanted chondrocytes, coupled with the inability of untreated chondral defects to repair or regenerate, demonstrates the utility of the canine model in evaluating novel materials for cartilage repair and regeneration.

Animals↗
PubMed1995

A general mechanism for transcriptional synergy by eukaryotic activators.

One of the important regulatory concepts to emerge from studies of eukaryotic gene expression is that RNA polymerase II promoters and their upstream activators are composed of functional modules whose synergistic action regulates the transcriptional activity of a nearby gene. Biochemical analysis of synergy by ZEBRA, a non-acidic activator of the Epstein-Barr virus (EBV) lytic cycle, showed that the synergistic transcriptional effect of promoter sites and activation modules correlates with assembly of the TFIID:TFIIA (DA) complex in DNase I footprinting and gel shift assays. The activator-dependent DA complex differs from a basal DA complex by its ability to bind TFIIB stably in an interaction regulated by TATA-binding protein-associated factors (TAFs). TFIIB enhances the degree of synergism by increasing complex stability. Similar findings were made with the acidic activator GAL4-VP16. Our data suggest a unifying mechanism for gene activation and synergy by acidic and non-acidic activators, and indicate that synergy is manifested at the earliest stage of preinitiation complex assembly.

DNA-Binding Proteins↗
PubMed1994

The Drosophila TIS11 homologue encodes a developmentally controlled gene.

We previously identified a murine primary response gene family containing three members; TIS11, TIS11B and TIS11D. Using degenerate oligonucleotides derived from conserved regions of the mouse TIS11 family cDNAs as primers and Drosophila genomic DNA as template for polymerase chain reaction amplification, we have identified a fly TIS11 homologue called DTIS11. The DTIS11 protein shares 90% sequence identity with the murine TIS11B and TIS11D proteins, over a 74 amino acid region that contains two CX8CX5CX3H repeated motifs separated by 18 amino acids. DTIS11 maps to region 11B(14-16) on the X-chromosome. Northern blot and in situ hybridization show that a maternal 3 kb message is present in embryos of early developmental stages. A 6 kb DTIS11 mRNA subsequently appears. In KC embryonal cells, both a strong 3 kb message and a less intense 6 kb message are present. The larger (6 kb) message is modestly induced in KC cells by both forskolin and tetradecanoyl phorbol acetate, and is stabilized by cycloheximide.

Amino Acid Sequence↗
PubMed1993

Ultrasound biomicroscopy in pseudophakic malignant glaucoma.

BACKGROUND: Malignant glaucoma (ciliary block glaucoma; aqueous misdirection glaucoma) is an incompletely understood, rare and serious complication of intraocular surgery. METHODS: A woman with pseudophakic malignant glaucoma underwent successful neodymium: YAG (Nd:YAG) laser photodisruption of the anterior hyaloid face with resolution of the glaucoma. High-resolution ultrasound biomicroscopy was used to image the anterior segment and anterior chamber angle before and after laser surgery. RESULTS: Ultrasound biomicroscopy provided cross-sectional images of the iris, posterior chamber intraocular lens (IOL), and ciliary body and their relative positions before and after resolution of the malignant glaucoma. Anterior rotation of the ciliary body and anterior chamber shallowing normalized after rupture of the anterior hyaloid face. CONCLUSION: High-resolution ultrasound biomicroscopy provided images consistent with accepted concepts of the pathophysiology of this disease and offers great promise for the future elucidation of the anatomic mechanisms underlying various forms of glaucoma.

Aged↗
PubMed1993

Comparing regions of the Epstein-Barr virus ZEBRA protein which function as transcriptional activating sequences in Saccharomyces cerevisiae and in B cells.

The ZEBRA protein activates expression of Epstein-Barr virus early-lytic-cycle genes in human B lymphocytes. Here it is shown that ZEBRA also behaves as a sequence-specific transcriptional activator in Saccharomyces cerevisiae. Deletional mutagenesis defined three regions of ZEBRA that participate in activation in S. cerevisiae. These regions are designated YI (amino acids [aa] 1 to 25), YII (aa 51 to 102), and YIII (aa 228 to 245). Two of the three regions of the native ZEBRA protein act together to mediate activation when assayed on ZEBRA binding sites. However, when fused to the DNA binding domain of GAL4 and assayed on GAL4 binding sites, regions YII and YIII were each sufficient to confer activation in S. cerevisiae. Regions of ZEBRA which affected activation in S. cerevisiae were also required in human B lymphocytes. The amino-terminal region of ZEBRA (aa 1 to 98) was required for activation both in S. cerevisiae and in human B cells; deletion of the carboxy-terminal 18 aa also significantly reduced activation in both cell types. Thus, the behavior of ZEBRA in human B cells and S. cerevisiae suggests that the protein contains universal activation motifs that interact with conserved components of the transcription machinery. However, certain deletion mutants of ZEBRA containing mutations in the N-terminal region exhibited discordant behaviors in S. cerevisiae and in B cells. For example, deletion of ZEBRA aa 26 to 51 impaired activation to a great extent in B cells but had little or no effect in S. cerevisiae. The discordant mutants may reflect interactions with a variable domain of a conserved component or unique interactions with specialized components of the basal transcription apparatus in different cells.

B-Lymphocytes↗
PubMed1993

The ZEBRA activation domain: modular organization and mechanism of action.

An RNA polymerase II activator often contains several regions that contribute to its potency, an organization ostensibly analogous to the modular architecture of promoters and enhancers. The regulatory significance of this parallel organization has not been systematically explored. We considered this problem by examining the activation domain of the Epstein-Barr virus transactivator ZEBRA. We performed our experiments in vitro so that the activator concentrations, stabilities, and affinities for DNA could be monitored. ZEBRA and various amino-terminal deletion derivatives, expressed in and purified from Escherichia coli, were assayed in a HeLa cell nuclear extract for the ability to activate model reporter templates bearing one, three, five, and seven upstream ZEBRA binding sites. Our data show that ZEBRA contains four modules that contribute to its potency in vitro. The modules operate interchangeably with promoter sites to determine the transcriptional response such that the loss of modules can be compensated for by increasing promoter sites. Potassium permanganate footprinting was used to show that transcriptional stimulation is a consequence of the activator's ability to promote preinitiation complex assembly. Kinetic measurements of transcription complex assembly in a reconstituted system indicate that ZEBRA promotes formation of a subcomplex requiring the TFIIA and TFIID fractions, where TFIIA acts as an antirepressor. We propose a model in which the concentration of DNA-bound activation modules in the vicinity of the gene initiates synergistic transcription complex assembly.

Cell Nucleus↗
PubMed1992

Age-related decline of disc rim area in visually normal subjects.

Optic disc parameters and axial lengths were measured in 81 visually normal young and elderly white adults (young [n = 41]: 27.2 +/- 5.7 years versus elderly [n = 40]: 68.8 +/- 8.4 years) using Rodenstock Optic Disc Analyzer and A-scan sonography. Axial lengths correlated positively with optic disc parameters (Spearman correlation analysis: rim area: P = 0.042, disc area: P = 0.052, and cup volume: P = 0.010). Older subjects had a shorter axial length (23.09 +/- 1.02 mm) and smaller disc rim area (1.171 +/- 0.338 mm2) than younger subjects (23.60 +/- 1.15 mm and 1.325 +/- 0.314 mm2; Mann-Whitney U test: P = 0.011 and P = 0.013, respectively). While both axial length and disc rim area declined with age (0.011 mm and 0.003 mm2 per year; Spearman correlation analysis: P = 0.032 and P = 0.020, respectively), the cup-to-disc and rim area-to-disc area ratios appeared to remain relatively constant throughout adult life. The age-related decline of disc rim area is consistent with histologic evidence of age-related decline of ganglion cell axons. The rim area-to-disc area ratio seems less affected by age, and is thus a better parameter to isolate age-related change from disease-related change of optic nerve in a longitudinal follow-up of diseases involving the optic nerve head.

Adolescent↗
PubMed1991

Optic nerve head and nerve fiber layer in Alzheimer's disease.

We compared (1) the differences in the retinal nerve fiber layer between 26 patients with Alzheimer's disease and 30 age- and race-matched normal controls with use of blue-light high-resolution photography, (2) the differences in disc pallor between 30 patients with Alzheimer's disease and 32 controls with use of a boundary-tracking program and fundus photographs, and (3) the topographic disc variables between 26 patients with Alzheimer's disease and 36 controls with use of an optic nerve head analyzer. A higher proportion of patients with Alzheimer's disease had detectable nerve fiber damage as seen by red-free photography compared with controls. Although the pallor area-to-disc area ratio was not significantly different between patients with Alzheimer's disease and controls, the patients with higher pallor area-to-disc area ratios had higher Alzheimer's Disease Assessment Scale (ADAS) scores and longer durations of disease. Patients had an increased cup-to-disc ratio and cup volume and decreased disc rim area compared with controls. These variables also correlated significantly with ADAS scores and the duration of disease. The correlation among the optic nerve head changes and the ADAS scores in patients with Alzheimer's disease suggests a potential role for optic nerve head analysis in monitoring the progression of Alzheimer's disease and in assessing the effectiveness of any treatments developed.

Aged↗