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S Yu

Publications and source records attributed to S Yu.

At least 109 records · Page 6Linked to original sources
PubMed2000

Characterization of a nuclear factor that binds to AP1-like element in the rat p53 promoter during liver regeneration.

The transcription level of the rat p53 gene increases at 5-12 h in the regenerating liver after partial hepatectomy. It was previously reported that an activator protein 1 (AP1)-like element (-264--284) mediated the induced transcription of the rat p53 gene during liver regeneration. In this study, we characterize the protein binding to the AP1-like element by various methods. Oligonucleotide competition assays showed that the binding protein did not require AP1 consensus sequence. Therefore, the binding protein is not an AP1 family protein. Zn(2+) was required for maximum DNA-binding activity of the protein, suggesting that the binding protein contains zinc fingers. The binding protein was highly resistant to denaturant. Even 1.8 M urea did not eliminate the protein-DNA complexes. In addition, the binding protein was stable up to 55 degrees C. The protein-DNA complexes were abolished in the presence of 0.6 M NaCl and higher. Protease clipping assay showed that the protein had a protease-resistant core DNA binding domain. These results provided new insights into the structure of the protein that binds to the AP1-like element of the p53 promoter during liver regeneration.

Animals↗
PubMed2000

1,5-Anhydro-D-fructose increases glucose tolerance by increasing glucagon-like peptide-1 and insulin in mice.

Besides being degraded to glucose-6-phosphate and to free glucose, glycogen is degraded by alpha-1,4-glucan lyase to 1, 5-anhydro-D-fructose. We examined the influence of 1, 5-anhydro-D-fructose on glucose-stimulated insulin secretion in vivo and in vitro in mice. When administered together with i.v. glucose (1 g/kg), 1,5-anhydro-D-fructose did not affect (at 0.2 g/kg) or inhibited (at 1 g/kg) insulin secretion without affecting glucose elimination. When incubated with isolated islets, 1, 5-anhydro-D-fructose at <16.7 mmol/l, did not affect glucose (11.1 mM)-stimulated insulin secretion but inhibited insulin secretion at 16.7 mmol/l. When given through a gastric gavage (150 mg/mouse) together with glucose (150 mg/mouse), 1,5-anhydro-D-fructose increased glucose tolerance and insulin secretion. Furthermore, 1, 5-anhydro-D-fructose potentiated the increase in plasma levels of the gut hormone, glucagon-like peptide-1 (GLP-1). We therefore conclude that when given enterally, but not parenterally, 1, 5-anhydro-D-fructose increases glucose tolerance in mice by increasing insulin secretion due to increased plasma levels of GLP-1. The sugar may therefore be explored for increasing endogenous GLP-1 secretion in the treatment of type 2 diabetes.

Animals↗
PubMed2000

Rab37 is a novel mast cell specific GTPase localized to secretory granules.

GTPases regulate a myriad of cellular functions including signal transduction, cytoskeletal organization and membrane trafficking. Rab GTPases act to coordinate the membrane dynamics of cells by organizing and regulating the activity of effector proteins important in vesicle trafficking. Rab37 is a novel Rab GTPase specifically expressed in the MC-9 mast cell line and bone marrow mast cells. Rab37 is 74% identical to Rab26 and 47% identical to Rab8, a GTPase important in Golgi to plasma membrane vesicle trafficking in mammalian cells. When green fluorescent protein tagged Rab37 is expressed in bone marrow mast cells, the secretory granules are labeled. These data suggest that Rab37 may play an important role in mast cell degranulation making this protein a potentially important target for therapeutic intervention in the treatment of allergy.

Amino Acid Sequence↗
PubMed2000

[Combined effects of lead and ethanol on rat sperms].

In order to study the combined effects of lead and ethanol on rat sperm, 54 male rats were divided into 9 groups randomly. One group was given distilled water as control, and the others (A-H) groups were given lead and ethanol at the concentrations of lead 11 mg/kgBW and lead 22 mg/kgBW, ethanol 0.9 g/kgBW, ethanol 1.8 g/kgBW, lead 11 mg/kgBW + ethanol 0.9 g/kgBW, lead 11 mg/kgBW + ethanol 1.8 g/kgBW, lead 22 mg/kgBW + ethanol 0.9 g/kgBW, lead 22 mg/kgBW + ethanol 1.8 g/kgBW in stomachs respectively for four weeks. The rats were sacrificed by the end of the fourth week. Epididymis were isolated and examined for sperm motility, counts and morphology. The results showed that the spermatozoa motility as well as spermatozoa count was lower; the spermatozoa morphological changed and blood lead level and ratio of epididymis to weight were higher in all combined experimental groups than those in groups with lead or ethanol alone. ANOVA analysis indicated that there were interaction between lead and ethanol on above indices (P < 0.05 P < 0.01). The multiple linear regression showed that there was linear correlation between blood lead and spermatozoa motility, spermatozoa morphological change. It is concluded that there were notable combined effects of lead and ethanol on semen quality in male rats.

Animals↗
PubMed2000

The kinetics of tolerance induction by nondepleting anti-CD4 monoclonal antibody (RIB 5/2) plus intravenous donor alloantigen administration.

BACKGROUND: CD4+ T cells play an essential role in allograft rejection. The monoclonal anti-rat CD4 antibody, RIB 5/2, has been shown to modulate the CD4 glycoprotein without eliminating the recipient T cells. We have successfully induced tolerance to rat heart allografts by recipient pretreatment with a single dose of RIB 5/2 plus intravenous administration of donor splenocytes. In this study, we explored whether this potent regimen could induce tolerance to the more resistant kidney and skin allografts. Furthermore, we examined the kinetics and requirements for tolerance to be met by a single dose of RIB 5/2 plus i.v. alloantigen. METHODS: The efficacy of a single i.p. dose of 20 mg/kg RIB 5/2 plus i.v. donor antigen (25x10(6) splenocyte) pretreatment 0, 21, or 40 days before receipt of an MHC-mismatched Lewis (RT1l) to Buffalo (RT1b) rat cardiac, renal, or skin allograft was studied. Another group of Buffalo recipients treated with RIB 5/2 plus an i.v. alloantigen +/-thymectomy received kidney transplants after 40 days. Attempts to prevent tolerance used interleukin-2 or prior sensitization. Mixed lymphocyte cultures, cytotoxic assays, and precursor frequencies of helper and cytotoxic cells, by limiting dilution analysis, serially measured in vitro cell-mediated immunity. RESULTS: RIB 5/2 administration combined with i.v. alloantigen 21 days before induced tolerance to heart and kidney allografts but did not prolong skin graft survival. In contrast, kidney allografts delayed for 40 days after pretreatment were acutely rejected and survival was not affected by the thymectomy. MLC, CTL, and pTH, and pCTL precursor frequencies from recipients of long-term grafts were specifically suppressed to donor, but not third party, alloantigen. CONCLUSION: A single dose of the nondepleting anti-CD4 monoclonal antibody, RIB 5/2, plus i.v. alloantigen is a potent inducer of tolerance to heart and kidney, but not skin, allografts. The RIB 5/2-induced donor unresponsiveness to a delayed kidney or cardiac allograft is time dependent but can be prolonged if specific alloantigen is present. Suppression of cell-mediated allo-immune responsiveness correlates with allograft acceptance.

Adoptive Transfer↗
PubMed2000

Brief cyclosporine treatment prevents intrathymic (IT) tolerance induction and precipitates acute rejection in an IT rat cardiac allograft model.

BACKGROUND: Intrathymic (IT) alloantigen combined with administration of rabbit anti-rat anti-lymphocyte serum (ALS) intraperitoneally induces donor-specific tolerance to rat cardiac transplants. The purpose of this study was to examine the effect of a brief course (4 days) of cyclosporine (CsA) on the development of IT tolerance. METHODS: Buffalo (BUF) (RT1b) rats were given 25x10(6) fully MHC-mismatched Lewis (LEW) (RT1l) splenocytes by IT injection plus 1.0 ml of ALS intraperitoneally. Twenty-one days later, IT donor-specific LEW (group 1) or third-party (ACI, RT1a) (group 2) hearts were heterotopically transplanted to the abdominal aorta A third group of BUF (group 3) were given daily CsA (10 mg/kg) by oral gavage for 4 days before administration of IT LEW cells and ALS. Rejection as defined by the cessation of a palpable heartbeat was confirmed by histology. Cytokine profiles of allografts from all groups were then analyzed using a multi-probe RNase protection assay. RESULTS: Sixty-seven percent of IT/ALS-treated BUF recipients not pretreated with CsA accepted LEW heart grafts for greater than 90 days. However, 86% of animals treated with CsA for 4 days before IT injection and ALS rejected allografts at 10.7+/-3.2 days. Third-party allografts (ACI) were uniformly rejected (7.0+/-0.0 days). Histology confirmed cellular rejection in CsA-treated allografts and cytokine analysis detected increased interleukin (IL)-3, IL-5, and tumor necrosis factor-alpha when compared to increased IL-2 and interferon-gamma in rejecting untreated controls. CONCLUSIONS: CsA can prevent the induction of intrathymic alloantigen tolerance. These results support the development of a CsA-sensitive, but IL-2-independent, active regulatory mechanism after intrathymic exposure to donor-specific alloantigen and depletion of mature peripheral T cells.

Animals↗
PubMed2000

Pharmacophore/receptor models for GABA(A)/BzR subtypes (alpha1beta3gamma2, alpha5beta3gamma2, and alpha6beta3gamma2) via a comprehensive ligand-mapping approach.

Pharmacophore/receptor models for three recombinant GABA(A)/BzR subtypes (alpha1beta3gamma2, alpha5beta3gamma2, and alpha6beta3gamma2) have been established via an SAR ligand-mapping approach. This study was based on the affinities of 151 BzR ligands at five distinct (alpha1-3,5,6beta3gamma2) recombinant GABA(A)/BzR receptor subtypes from at least nine different structural families. Examination of the included volumes of the alpha1-, alpha5-, and alpha6-containing subtypes indicated that region L(2) for the alpha5-containing subtype appeared to be larger in size than the analogous region of the other receptor subtypes. Region L(Di), in contrast, appeared to be larger in the alpha1 subtype than in the other two subtypes. Moreover, region L(3) in the alpha6 subtype is either very small or nonexistent in this diazepam-insensitive subtype (see Figure 16 for details) as compared to the other subtypes. Use of the pharmacophore/receptor models for these subtypes has resulted in the design of novel BzR ligands (see 27) selective for the alpha5beta3gamma2 receptor subtype. alpha5-Selective ligand 27 when injected directly into the hippocampus did enhance memory in one paradigm (Bailey et al., unpublished observations); however, systemic administration of either 9 or 27 into animals did not provide an observable enhancement. This result is in complete agreement with the observation of Liu (1996). It has been shown (Liu, 1996; Wisden et al., 1992) that in the central nervous system of the rat (as well as monkeys and pigeons) there are several native subtypes of the GABA(A) receptor which exhibit different functions, regional distributions, and neuronal locations. Although 27 binds more potently at alpha5beta3gamma2 receptor subtypes and is clearly an inverse agonist (Liu et al., 1996; Liu, 1996), it is possible that this ligand acts as an agonist at one or more subtypes. Liu (1996) clearly showed that a number of imidazobenzodiazepines were negative modulators at one subtype and agonists at another. Therefore, selectivity for a particular subtype at this point is not sufficient to rule out some physiological effect at other GABA(A)/BzR subtypes. The inability of 27 to potentiate memory when given systemically is again in support of this hypothesis, especially since alpha1beta2gamma2 subtypes are distributed throughout the brain (Wisden et al., 1992). A drug delivered systemically is far more likely to interact with all subtypes than one delivered to a specific brain region. This observation (systemic vs intrahippocampal) provides further support for the design of more subtype-specific ligands at the BzR to accurately define their pharmacology, one key to the design of new drugs with fewer side effects.

Animals↗
PubMed2000

Biochemical characterization of a nuclear factor that binds to NF1-like elements in the rat p53 promoter.

We previously reported that two nuclear factor 1-like elements mediated the transcription of the rat p53 gene. A 40-kDa protein was shown to bind to these elements, which was different from common NF1 family proteins. In this study, the biochemical properties of the 40-kDa binding protein were investigated. The metal ion dependency of the protein was examined with various chelators; the protein was proved to require Mg(2+) for maximum DNA-binding activity. The binding protein was highly resistant to ionic strength and denaturant. The protein-DNA complex was reduced at high NaCl concentration, but residual DNA-binding activity remained. Even 2 M urea did not completely eliminate the formation of protein-DNA complex. DNA-binding activity of the protein was also stable at high temperature. Treatment of the protein-DNA complex with increasing concentrations of proteinase K or trypsin demonstrated the existence of a protease-resistant DNA-bound core. These biochemical properties provide new insight into the 40-kDa NF1-like nuclear factor.

Animals↗
PubMed2000

Significance of protein kinase CK2 nuclear signaling in neoplasia.

Many stimuli play a role in influencing the structure and function of chromatin and nuclear matrix through post-translational modifications of the component proteins in these dynamic structures. We propose that the protein serine/threonine kinase CK2 (formerly casein kinase II) is one such agent that is involved in signal transduction in the nuclear matrix and chromatin in response to a variety of stimuli. Protein kinase CK2 appears to undergo rapid modulations in its association with nuclear matrix and nucleosomes in response to mitogenic signals and is involved in the phosphorylation of a variety of intrinsic proteins in these structures depending on the state of genomic activity. In addition, its association or loss from the nuclear matrix may also influence the apoptotic activity in the cell. CK2 has been found to be dysregulated in virtually all the neoplasias examined and nuclear association appears to be an important facet of its expression in tumor cells. We hypothesize that CK2 provides a functional paradigm linking the nuclear matrix and chromatin structures. Identification of precise loci of action of CK2 in these structures and how they influence the morphological appearance of the nucleus under normal and abnormal growth conditions would be an important future direction of investigation. J. Cell. Biochem. Suppl. 35:130-135, 2000. Published 2001 Wiley-Liss, Inc.

Animals↗
PubMed2000

Protective effects of radix astragali against anoxic damages to in vitro cultured neurons.

To study the protective effects of radix astragali against anoxic damages to in vitro cultured neurons in rats, NaCN was used to develop a hypoxic model of in vitro cultured neurons from newborn rat cerebral cortex. The cellular morphology, A value (cell survival number) and effluxes of lactate dehydrogenase (LDH) and K+ from cells were measured in the radix astragali group and the control group respectively. After 48 h of anoxia, A value was decreased from 0.325 +/- 0.031 before anoxia to 0.145 +/- 0.011, the effluxes of LDH and K+ were increased from 65.80 +/- 2.90 U/L and 5. 23 +/- 0.11 mmol/L before anoxia to 148.80 +/- 8.40 U/L and 7.31 +/- 0.18 mmol/L, respectively. It was found that in the anoxic circumstance in the Radix astragali group, the mophological changes were mild, the effluxes of LDH and K+ were decreased and A value increased as compared with those in the control group. It was suggested that Radix astragali could protect the cultured rat neurons against anoxic damages in the anoxic circumstance.

Animals↗
PubMed2000

Preliminary study of stereotactic radiotherapy for lung cancer.

From March 1997 to November 1999, 45 patients with lung cancer were treated by a stereotactic radiotherapy, with 15 cases treated by a stereotactic radiotherapy alone, and 30 cases by the external radiotherapy plus stereotactic radiotherapy. The clinical target volume was 1.89-187.26 cm3 with the median being 18.17 cm3. The doses of plan target volume (PTV) edge was 16-30 Gy/2-3 times and the doses of center was 120% to 150% of PTV edge doses. The overall response rate was 84.4% (38/45), with 11 complete response (CR) and 27 partial response (PR). This study confirmed that the stereotactic radiotherapy is a safe and effective therapy for lung cancer. For those early-stage patients who can tolerate neither operation nor even conventional radiotherapy for various reasons, it can both achieve therapeutic purpose and improve quality of life.

Adenocarcinoma↗
PubMed2000

A novel mutation in a family with non-erythroid variant form of acute intermittent porphyria.

Acute intermittent porphyria (AIP), an autosomal dominant disorder, is divided into two forms, the classical form (more than 95%) and the non-erythroid variant form, according to erythroid porphobilinogen deaminase (PBGD) activity. In the variant form, the PBGD activity is essentially normal. Detection of presymptomatic mutation carriers relies on a DNA test. This variant form of AIP is very rare, with only nine families carrying five different mutations reported in the literature. Here we report a novel G-to-T transversion in the first position of intron 1 of the PBGD gene in a family with this variant form of AIP. We also review all previously reported cases and propose an effective diagnostic approach.

Adult↗
PubMed2000

Production of monoclonal antibody to deltorphin-I and its immunocytochemical application to adult rat brain and cultured rat brain neurons.

A monoclonal anti-deltorphin-I antibody specifically recognizing its NH2-terminal region was produced. In the adult rat brain sections, it recognized immunoreactive nerve fibers mainly in the bed nucleus of stria terminalis, central nucleus of amygdala, lateral hypothalamus, hippocampus, substantia nigra, periaqueductal gray and locus ceruleus. Occasionally, positive somata were localized in the bed nucleus of stria terminalis, central nucleus of amygdala, supraoptic and periventricular nuclei. In primarily cultured neurons from various brain regions of new-born rats, the antibody immunostained strongly neuronal somata and processes. The abundant DADTI-immunoreactive substance in the cultured neurons promises to provide an alternative pathway to search for the counterpart of deltorphins in mammals.

Amygdala↗
PubMed2000

Polymorphisms in the CAG repeat--a source of error in Huntington disease DNA testing.

Five of 400 patients (1.3%), referred for Huntington disease DNA testing, demonstrated a single allele on CAG alone, but two alleles when the CAG + CCG repeats were measured. The PCR assay failed to detect one allele in the CAG alone assay because of single-base silent polymorphisms in the penultimate or the last CAG repeat. The region around and within the CAG repeat sequence in the Huntington disease gene is a hot-spot for DNA polymorphisms, which can occur in up to 1% of subjects tested for Huntington disease. These polymorphisms may interfere with amplification by PCR, and so have the potential to produce a diagnostic error.

Adult↗
PubMed2000

Protection of Rpe65-deficient mice identifies rhodopsin as a mediator of light-induced retinal degeneration.

Light-induced apoptosis of photoreceptors represents an animal model for retinal degeneration. Major human diseases that affect vision, such as age-related macular degeneration (AMD) and some forms of retinitis pigmentosa (RP), may be promoted by light. The receptor mediating light damage, however, has not yet been conclusively identified; candidate molecules include prostaglandin synthase, cytochrome oxidase, rhodopsin, and opsins of the cones and the retinal pigment epithelium (PE). We exposed to bright light two groups of genetically altered mice that lack the visual pigment rhodopsin (Rpe65-/- and Rho-/-). The gene Rpe65 is specifically expressed in the PE and essential for the re-isomerization of all-trans retinol in the visual cycle and thus for the regeneration of rhodopsin after bleaching. Rho-/- mice do not express the apoprotein opsin in photoreceptors, which, consequently, do not contain rhodopsin. We show that photoreceptors lacking rhodopsin in these mice are completely protected against light-induced apoptosis. The transcription factor AP-1, a central element in the apoptotic response to light, is not activated in the absence of rhodopsin, indicating that rhodopsin is essential for the generation or transduction of the intracellular death signal induced by light.

Animals↗