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Y Chang

Publications and source records attributed to Y Chang.

At least 73 records · Page 4Linked to original sources

[Shoulder pain after laparoscopic cholecystectomy].

OBJECTIVE: To detect the mechanism of shoulder pain after laparoscopic cholecystectomy(LC). METHODS: Ninety patients who had receive LC were randomly divided into three groups (each 30 patients): group A, no management after LC; group B, absorption of residual CO2 after LC; group C, O2 insufflation for three times followed by complete absorption of CO2 after LC. PO2 and PCO2 before and after LC were recorded. Postoperative shoulder pain was assessed with shoulder pain's rate and level. RESULTS: The PO2 difference of group C between before and after LC was significant as compared to groups A and B(P < 0.05). Postoperative shoulder pain developed in 13 patients (43.33%) of group A, in 8 (26.67%) of group B, and 21 (70%) of group C (P > 0.05 A vs B; P < 0.05 A vs C; and P < 0.01 B vs C). The shoulder pain's level was higher in group C than in groups A and B. CONCLUSIONS: Direct irritation to the diaphragm due to the residual CO2 pneumoperitoneum is not the main cause of shoulder pain. The excessive traction of the triangular ligament and over-stretching of the diaphragmatic fibers due to insufflation are the main cause of shoulder pain.

Carbon Dioxide↗

The scid recombination-inducible cell line: a model to study DNA-PK-independent V(D)J recombination.

To investigate the molecular mechanisms of the variable (diversity) joining (V(D)J) recombination process at an endogenous gene locus, recombination-inducible cell lines were made from both bcl-2-bearing severe combined immune deficiency (scid) homozygous and scid heterozyous (s/ + ) mice by transforming pre-B cells with the temperature-sensitive Abelson murine leukemia virus (ts-Ab-MLV). These transformants can be induced to undergo immunoglobulin light-chain gene rearrangements by incubating them at the non-permissive temperature. In the case of transformed scid cells, a significant amount of hairpin coding ends are accumulated during recombination induction, but few coding joints are generated. After being shifted to the permissive temperature. however, these cells are capable of opening hairpin ends and forming coding joints. Thus, ts-Ab-MLV transformed scid cells can be readily manipulated for both recombination cleavage and end resolution. However, unlike the rapid coding joint formation in s/ + cells that have the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs), the process for resolving coding ends in scid cells is slow and error prone, and also appears to be correlated with a reduction in the RAG1/2 expression. Apparently, this process is mediated by a DNA-PK-independent pathway. The fact that the activity of this pathway can be manipulated in vitro makes it possible to delineate the mechanisms in end opening, processing and joining. Therefore, these ts-Ab-MLV transformed scid cell lines offer a model to study the molecular nature as well as the regulation of the DNA-PK-independent pathway in coding end resolution.

Animals↗

The effects of ligand binding on the backbone dynamics of the kringle 1 domain of human plasminogen.

The internal motions of the backbone nitrogen atoms of the kringle 1 domain of human plasminogen (K1(Pg)) were examined in the absence and presence of the ligand, epsilon-aminocaproic acid. These dynamic properties were determined from (15)N NMR relaxation data in terms of the extended model-free parameters. The model of isotropic reorientation was found sufficient to account for overall molecular tumbling for both apo and EACA-bound K1(Pg). The global rotational correlation time (tau(m)) for apo-K1(Pg) was 5.87(+/-0.01) ns, while the tau(m) for ligand-bound K1(Pg) was 5.20(+/-0.01) ns, suggesting that perhaps some small degree of aggregation occurred in the apo form of the kringle module. Complexation of K1(Pg) with ligand mainly reduced those internal motions that occurred on a 100 ps to 5 ns time-scale. The magnitude of the chemical exchange was also attenuated upon ligand binding. These data are consistent with studies employing other approaches that suggest that the binding pocket is preformed in K1(Pg).

Aminocaproic Acid↗

Implications of stroke risk criteria on the anticoagulation decision in nonvalvular atrial fibrillation: the Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA) study.

BACKGROUND: Warfarin dramatically reduces the risk of stroke in patients with nonvalvular atrial fibrillation (NVAF) but increases the likelihood of bleeding. Accurately identifying patients who need anticoagulation is critical. We assessed the potential impact of prominent stroke risk classification schemes on this decision in a large sample of patients with NVAF. METHODS AND RESULTS: We used clinical and electrocardiographic databases to identify 13 559 ambulatory patients with NVAF from July 1996 through December 1997. We compared the proportion of patients classified as having a low enough stroke risk to receive aspirin using published criteria from the Atrial Fibrillation Investigators (AFI), American College of Chest Physicians (ACCP), and the Stroke Prevention in Atrial Fibrillation Investigators (SPAF). In this cohort, AFI criteria classified 11% as having a low stroke risk, compared with 23% for ACCP and 29% for SPAF (kappa range, 0.44 to 0.85). This 2- to-3-fold increase in low stroke risk patients by ACCP and SPAF criteria primarily resulted from the inclusion of many older subjects (65 to 75 years+/-men >75 years) with no additional clinical stroke risk factors. CONCLUSIONS: The age threshold for assigning an increased stroke risk has a dramatic impact on whether to recommend warfarin in populations of patients with NVAF. Large, prospective studies with many stroke events are needed to precisely determine the relationship of age to stroke risk in AF and to identify which AF subgroups are at a sufficiently low stroke risk to forego anticoagulation.

Aged↗

Evaluation of the latency-associated nuclear antigen (ORF73) of Kaposi's sarcoma-associated herpesvirus by peptide mapping and bacterially expressed recombinant western blot assay.

Kaposi's sarcoma (KS)-associated herpesvirus open-reading frame (ORF) 73 encodes a latency-associated nuclear antigen (LANA) that is the basis for several serologic assays. Immunoreactive epitopes were searched for by peptide mapping, and 171 cleavable, biotinylated 17-mer peptides offset by 5 residues were synthesized and screened with human serum samples by ELISA. The initial screen, which used highly reactive serum diluted 1:500, identified 38 immunoreactive peptides. These were subsequently tested on additional serum samples diluted 1:40. Thirteen peptides were more reactive with serum samples from patients with KS than with control serum samples. No single epitope was recognized by most KS patient serum samples. Combined use of these peptides did not increase test sensitivity to that of current indirect immunofluorescence assays for LANA (80%-90%). For comparison, full-length ORF73 was expressed in bacteria and analyzed by Western blot. The overall sensitivity was 67% (range, 100% among US patients with classic KS to 52% among Italian patients with classic KS). These studies suggest that LANA immunoreactivity may be due to variations in patient response or conformational epitopes.

Antigens, Viral↗

Hrs-2 regulates receptor-mediated endocytosis via interactions with Eps15.

Hrs-2, via interactions with SNAP-25, plays a regulatory role on the exocytic machinery. We now show that Hrs-2 physically interacts with Eps15, a protein required for receptor-mediated endocytosis. The Hrs-2/Eps15 interaction is calcium dependent, inhibited by SNAP-25 and alpha-adaptin, and results in the inhibition of receptor-mediated endocytosis. Immunoelectron microscopy reveals Hrs-2 localization on the limiting membrane of multivesicular bodies, organelles in the endosomal pathway. These data show that Hrs-2 regulates endocytosis, delineate a biochemical pathway (Hrs-2-Eps15-AP2) in which Hrs-2 functions, and suggest that Hrs-2 acts to provide communication between endo- and exocytic processes.

Adaptor Proteins, Signal Transducing↗

Metabolism of recombination coding ends in scid cells.

V(D)J recombination cleavage generates two types of dsDNA breaks: blunt signal ends and covalently sealed hairpin coding ends. Although signal ends can be directly ligated to form signal joints, hairpin coding ends need to be opened and subsequently processed before being joined. However, the underlying mechanism of coding end resolution remains undefined. The current study attempts to delineate this process by analyzing various structures of coding ends made in situ from recombination-inducible pre-B cell lines of both normal and scid mice. These cell lines were derived by transformation of B cell precursors with the temperature-sensitive Abelson murine leukemia virus. Our kinetic analysis revealed that under conditions permissive to scid transformants, hairpin coding ends could be nicked to generate 3' overhangs and then processed into blunt ends. The final joining of these blunt ends followed the same kinetics as signal joint formation. The course of this process is in sharp contrast to coding end resolution in scid heterozygous transformants that express the catalytic subunit of DNA-dependent protein kinase, in which hairpin end opening, processing, and joining proceeded very rapidly and appeared to be closely linked. Furthermore, we demonstrated that the opening of hairpin ends in scid cells could be manipulated by different culture conditions, which ultimately influenced not only the level and integrity of the newly formed coding joints, but also the extent of microhomology at the coding junctions. These results are discussed in the context of scid leaky recombination.

Animals↗

Characterization of the sialidase molecular defects in sialidosis patients suggests the structural organization of the lysosomal multienzyme complex.

Sialidosis is an autosomal recessive disease caused by the genetic deficiency of lysosomal sialidase, which catalyzes the hydrolysis of sialoglycoconjugates. The disease is associated with progressive impaired vision, macular cherry-red spots and myoclonus (sialidosis type I) or with skeletal dysplasia, Hurler-like phenotype, dysostosis multiplex, mental retardation and hepatosplenomegaly (sialidosis type II). We have analyzed the genomic DNA from nine sialidosis patients of multiple ethnic origin in order to find mutations responsible for the enzyme deficiency. The activity of the identified variants was studied by transgenic expression. One patient had a frameshift mutation (G623delG deletion), which introduced a stop codon, truncating 113 amino acids. All others had missense mutations: G679G-->A (Gly227Arg), C893C-->T (Ala298Val), G203G-->T (Gly68Val), A544A-->G (Ser182Gly) C808C-->T (Leu270Phe) and G982G-->A (Gly328Ser). We have modeled the three-dimensional structure of sialidase based on the atomic coordinates of the homologous bacterial sialidases, located the positions of mutations and estimated their potential effect. This analysis showed that five mutations are clustered in one region on the surface of the sialidase molecule. These mutations dramatically reduce the enzyme activity and cause a rapid intralysosomal degradation of the expressed protein. We hypothesize that this region may be involved in the interface of sialidase binding with lysosomal cathepsin A and/or beta-galactosidase in their high-molecular-weight complex required for the expression of sialidase activity in the lysosome.

Adolescent↗

Kaposi's sarcoma.

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Acquired Immunodeficiency Syndrome↗

KSHV-encoded CC chemokine vMIP-III is a CCR4 agonist, stimulates angiogenesis, and selectively chemoattracts TH2 cells.

Kaposi's sarcoma-associated herpesvirus (KSHV) encodes 3 genes that are homologous to cellular chemokines. vMIP-III, the product of open reading frame K4.1, is the most distantly related to human chemokines and has yet to be characterized. We have examined the interaction of vMIP-III with chemokine receptors, its expression in KS lesions, and its in ovo angiogenic properties. We show expression of vMIP-III in KS lesions and demonstrate the stimulation of angiogenesis by this chemokine, like vMIP-I and vMIP-II, in the chick chorioallantoic membrane assay. vMIP-III does not block human immunodeficiency virus entry through the coreceptors CCR3, CCR5, or CXCR4. However, vMIP-III is an agonist for the cellular chemokine receptor CCR4. CCR4 is expressed by TH2-type T cells. Consistent with this, vMIP-III preferentially chemoattracts this cell type. Because of these biologic properties and because it is expressed in KS lesions, vMIP-III may play an important role in the pathobiology of KS. (Blood. 2000;95:1151-1157)

Allantois↗

Caveolar structure and protein sorting are maintained in NIH 3T3 cells independent of glycosphingolipid depletion.

Glycosphingolipids have been proposed to be critical components of clustered lipids within cell membranes that serve as rafts for the attachment and sorting of proteins to the cell membrane. Density gradient centrifugation was used to isolate and to ascertain the lipid composition of caveolin-enriched membranes. These membranes demonstrated a significant enrichment of sphingolipids and cholesterol containing up to 20 and 30%, respectively, of the cellular glucosylceramide and lactosylceramide. A specific inhibitor of glucosylceramide synthase, d-threo-1-phenyl-2-palmitoyl-3-pyrrolidino-propanol, was used to test the hypothesis that glycosphingolipids are required for the sorting of proteins to caveolae. When NIH 3T3 cells were depleted of their glucosylceramide based glycosphingolipid mass, the caveolar structure remained intact as determined by electron microscopy and confocal microscopy. The caveolar proteins caveolin and annexin II sorted normally to caveolae, as determined by immunoblotting and confocal microscopy. When the GPI-linked protein B61 was inducibly expressed in these cells, sorting to caveolar membranes occurred normally, even in the presence of glucosylceramide depletion. These observations suggest that protein sorting to caveolae in fibroblasts occurs independently of glycosphingolipid synthesis.

3T3 Cells↗

308-nm excimer laser for the treatment of psoriasis: a dose-response study.

OBJECTIVE: To determine the dose-response relationship of excimer laser-generated 308-nm UV-B radiation for treating psoriasis. DESIGN: Pilot study with a before-after design. SETTING: A university dermatology service. PATIENTS: Thirteen consecutive patients with at least 4 large, stable psoriasis plaques. INTERVENTIONS: Excimer laser-generated 308-nm UV-B radiation was given to each of 4 plaques, which received 1, 2, 4, and 20 treatments, respectively. Untreated areas within each plaque served as controls. Within each plaque, 8 doses based on multiples of a predetermined minimal erythema dose (MED) were tested in distinct sites. The multiples were 0.5 and 1 (low dose); 2, 3, 4, and 6 (medium dose); and 8 and 16 (high dose). At every treatment, the dose for each site remained fixed at the same MED multiple. A psoriasis severity index score was determined for each area before, every 2 weeks during, and 2 and 4 months after treatment. RESULTS: The mean+/-SD MED was 203.03+/-57.84 mJ/ cm2. Treatment with high fluences produced significantly better results than that with medium and low fluences at weeks 4, 6, 8, and 10 (P<.05). At 4 months' follow-up, all sites that received low or medium fluences had recurrences, whereas those that underwent a single treatment at 8 and 16 MED multiples remained in remission. CONCLUSIONS: With 308-nm UV-B radiation generated by an excimer laser, it is possible to clear psoriasis with as little as 1 treatment with moderately long remission. In contrast to traditional phototherapy techniques, this handheld excimer laser UV-B therapy is selectively directed toward lesional skin, thus sparing the surrounding normal skin from unnecessary radiation exposure. Treatment of other inflammatory diseases and limited psoriasis seems reasonable to pursue with this modality.

Dose-Response Relationship, Radiation↗

Diffusion-weighted magnetic resonance imaging identifies the "clinically relevant" small-penetrator infarcts.

BACKGROUND: Most patients initially seen with a clinical syndrome consistent with a small-penetrator infarct (SPI) also harbor multiple, chronic, hyperintense, white matter lesions on conventional magentic resonance imaging (ie, T2-weighted image [T2WI] and fluid-attenuation inversion recovery [FLAIR] imaging). Diffusion-weighted imaging (DWI) can identify the clinically relevant "index infarction" in such circumstances, since it differentiates between acute and chronic lesions. OBJECTIVE: To determine the clinical and radiological predictors associated with misidentification of an SPI as acute using T2WI and FLAIR images in patients with an acute SPI seen on DWI. PATIENTS: Sixty-seven consecutive patients who had an SPI. METHODS: Two independent examiners, provided with brief clinical information, but blinded to DWI findings, sought a clinically appropriate lesion on T2WI and FLAIR imaging in 67 consecutive patients found to have an SPI seen on DWI. RESULTS: The index infarction based on evaluation of T2WI or FLAIR images was in a different location than the acute lesion as identified by DWI in 9 (13%) and 11 (16%) of 67 patients, respectively. Both T2WI and FLAIR imaging were rated normal in another 9% of the patients. Multivariate analysis showed that small lesion size (<10 mm) was the only predictor of misidentifying the clinically appropriate lesion on conventional magnetic resonance imaging (P<.01). CONCLUSIONS: T2-weighted imaging and FLAIR imaging fail to identify the clinically relevant SPI in almost one quarter of the patients found to have a lesion on DWI. The characteristics of DWI make it well suited for the detection of acute small infarcts. Diffusion-weighted imaging is necessary to consistently define the clinical-anatomical relations in patients initially seen with SPIs.

Adult↗

Study on fragmentation behavior of 5/7/6-type taxoids by tandem mass spectrometry.

The mass spectrometric behaviors of seven compounds, namely four 4beta(20),5-oxetane 5/7/6-type taxoids (i.e. taxayuntin A, taxayuntin B, taxayuntin and taxayuntin C) and three 4(20)-methylene 5/7/6-type taxoids (i.e. brevifoliol, taxchinin A and 7-acetyl-10-deacetyl-7-debenzoylbrevifoliol) have been investigated by the positive ion FAB-MS/MS technique. The fragmentation has been correlated with the types and positions of substituents of these compounds. It has been found that with the OH group at the C-10 position, taxayuntin A, taxayuntin B and 7-acetyl-10-deacetyl-7-debenzoylbrevifoliol are dominated by the loss of H2O, while with the BzO group at the C-10 position, taxayuntin, taxayuntin C, brevifoliol and taxchinin A preferentially eliminate the BzO group. In addition, C-2 is an active site, and neutral loss from the C-2 position readily occurs. The four 4beta(20),5-oxetane 5/7/6-type taxoids produce the terminal product ion with a stable conjugated system at m/z 311, while the 4(20)-methylene 5/7/6-type taxoids brevifoliol and 7-acetyl-10-deacetyl-7-debenzoylbrevifoliol produce this ion at m/z 237, and taxchinin A at m/z 253. Interestingly, characteristic fragment ions involving the loss of a 118 u group were observed for taxayuntin, and a possible fragmentation mechanism is given. The major fragmentation pathways and mechanisms of ion formation for the compounds are proposed on the basis of CID spectra and accurate mass measurements. The results of this paper will be helpful for structural analysis of analogs.

Plant Extracts↗

Fixation of biological tissues with a naturally occurring crosslinking agent: fixation rate and effects of pH, temperature, and initial fixative concentration.

In an attempt to overcome the cytotoxicity problem of the glutaraldehyde-fixed tissues, a naturally occurring crosslinking agent (genipin) was used by our group to fix biological tissues. The study was intended to investigate the rate of tissue fixation by genipin. Glutaraldehyde was used as a control. In addition, the degrees of tissue fixation by genipin at different pHs (pH 4.0, pH 7. 4, pH 8.5, or pH 10.5), temperatures (4 degrees C, 25 degrees C, 37 degrees C, or 45 degrees C), and initial fixative concentrations (0.250%, 0.625%, or 1.000%) were examined. The results obtained revealed that the rate of tissue fixation by glutaraldehyde was significantly faster than that by genipin. The degree of tissue fixation by genipin may be controlled by adjusting its fixation duration or fixation conditions. The order in degree of tissue fixation by genipin at different pHs, from high to low, was: at nearly neutral pH (pH 7.4 or pH 8.5) > at basic pH (pH 10.5) > at acidic pH (pH 4.0). The degrees of tissue fixation by genipin at different temperatures were about the same, except for that at 4 degrees C. In contrast, the initial fixative concentration did not seem to affect the degree of tissue fixation by genipin, if only the amount of genipin in the fixation solution was sufficient to complete tissue fixation. The concentrations of genipin in the aqueous solutions at different pHs, temperatures, and initial fixative concentrations tended to decrease with time with or without the occurrence of tissue fixation. This indicated that genipin was not stable in the aqueous solution. The instability of aqueous genipin was more remarkable with increasing pH or temperature. The results obtained in this study may be used to optimize the fixation process for developing bioprostheses fixed by genipin.

Animals↗

Extended alternating-temperature cold acclimation and culture duration improve pear shoot cryopreservation.

Meristems of many pear genotypes can be successfully cryopreserved following 1 week of cold acclimation, but an equal number do not survive the process or have very little regrowth. This study compared commonly used cold acclimation protocols to determine whether the cold acclimation technique used affected the cold hardiness of shoots or the regrowth of cryopreserved meristems. In vitro-grown pear (Pyrus L.) shoots were cold acclimated for up to 16 weeks, then either the shoot tips were tested for cold hardiness or the meristems were cryopreserved by controlled freezing. Cold acclimation consisted of alternating temperatures (22 degrees C with light/-1 degrees C darkness with various photo- and thermoperiods) or a constant temperature (4 degrees C with an 8-h photoperiod or darkness). Compared with nonacclimated controls, both alternating- and constant-temperature acclimation significantly improved postcryopreservation regrowth of P. cordata Desv. and P. pashia Buch. -Ham. ex D. Don meristems. Alternating-temperature acclimation combined with either an 8-h photoperiod or darkness was significantly better than constant-temperature acclimation. Alternating-temperature shoot acclimation for 2 to 5 weeks significantly increased postcryopreservation meristem regrowth, and recovery remained high for up to 15 weeks acclimation. Postcryopreservation meristem regrowth increased with 1 to 5 weeks of constant-temperature acclimation and then declined with longer acclimation. Shoot cold hardiness varied with the acclimation procedure. The LT(50) of shoots acclimated for 10 weeks with alternating temperatures was -25 degrees C; that with constant temperature was -14.7 degrees C; and that of the nonacclimated control was -10 degrees C. Less frequent transfer of cultures also improved acclimation of shoots. Shoots grown without transfer to fresh medium for 6-12 weeks had higher postcryopreservation recovery with shorter periods of acclimation than shoots with a 3-week transfer cycle.

Acclimatization↗

Differential viral protein expression in Kaposi's sarcoma-associated herpesvirus-infected diseases: Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman's disease.

Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is linked to KS, primary effusion lymphomas (PEL), and a subset of multicentric Castleman's disease (MCD). Transcript mapping studies using PEL cell lines have allowed preliminary classification of viral gene expression into constitutive (class I) and inducible (class II/III) categories. To determine whether viral gene expression differs in vivo, we examined tissue sections of KSHV-infected disorders, using specific antibodies against proteins that are representative of the different expression classes of KSHV genes. ORF73/LANA appears to be a surrogate marker for KSHV infection because it is constitutively expressed in vitro and in vivo in all KSHV-infected cells. Expression of vIRF1, vIL6, and PF-8 proteins in the infected B cells of MCD lymph nodes reproduces the expression pattern observed in TPA-stimulated KSHV-infected B-cell lines. In contrast, the protein expression of the inducible viral genes that we tested in KS and PEL biopsies is restricted to PF-8 and vIL6, respectively. The tightly restricted expression of KSHV proteins in vivo differs from the dysregulated expression of inducible KSHV genes in vitro and suggests that viral gene expression in KSHV-infected cell lines does not accurately reflect what occurs in diseased tissues. These differences may be related to either cell-specific or immune restriction of viral replication.

Castleman Disease↗