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Biomedical subjects

A Yu

Publications and source records attributed to A Yu.

At least 55 records · Page 3Linked to original sources
PubMed1999

[Effects of Chinese patent medicine tongfugushen on adenine-induced chronic renal failure in rats].

OBJECTIVE: To observe the effects of Tongfugushen(TFGS) on adenine-induced chronic renal failure in rats. METHODS: The model of chronic renal failure was made by feeding rats with food containing 0.5% adenine. Two weeks later, along with the above food, the treated group was administered the Chinese patent medicine TFGS, and the control group was given NS. Blood tests including urea nitrogen(BUN), serum creatinine(Scr), red blood cell(RBC), hemoglobin (Hb), hematocrit(HCT) and renal pathological tests were performed at the end of the fourth week. RESULT: In the TFGS treated group, the mean levels of BUN and Scr were lower and the mean values of RBC, Hb and HCT were higher than those in the control group, and the deposited crystals of adenine metabolite and the proliferation of fibroid tissue in kidney were decreased. CONCLUSION: TFGS is helpful in improving the symptoms of chronic renal failure in rats.

Adenine↗
PubMed1998

Contrasting effects of inflammatory cytokines and glucocorticoids on the production of activin A in human marrow stromal cells and their implications.

Human marrow stromal cells were analysed with immunocytochemical staining, Northern blot, and functional bioassay for production of activin A. Although Northern blot and immunocytochemical staining did not detect the alpha subunit of inhibin in human marrow stromal cells, RT-PCR analyses confirmed its presence, along with the expected activin beta A PCR products. Present studies showed that human marrow fibroblastoid cells were reactive with anti-activin A antibodies and that the production of beta A RNA was upregulated by pro-inflammatory cytokines/regulators like interleukin 1 alpha (IL-1 alpha), tumour necrosis factor-alpha (TNF-alpha), lipopolysaccharide (LPS) or 12-O-tetradecanoylphorbol 13-acetate (TPA). IL-1 alpha or TNF-alpha stimulated-marrow stromal cells accumulated beta A RNA after 2 h of incubation, reaching a peak stimulation at approximately 8 h. Biologically active activin A molecules were detected in the conditioned media by a bioassay, and their activity was specifically inhibited by a blocking antibody or an activin-binding protein, follistatin. Accumulation of bioactive activin A in conditioned medium of human marrow stromal cells increased after incubation with IL-1 alpha or TNF-alpha. Nuclear run-off assays with TNF-alpha stimulated marrow stromal cells showed that the enhanced expression of activin A was related to an increase in its rate of transcription. In contrast to the stimulatory effect of pro-inflammatory cytokines, hydrocortisone and dexamethasone at 1 x 10(-7) to 1 x 10(-6) M inhibited both the constitutive and the cytokine-stimulated expression of activin beta A RNA, and also the production of bioactive activin A protein. The upregulation of activin A production by cytokines and its suppression by glucocorticoids imply that activin A may also act as a moderator in diverse functions including host defences.

Activins↗
PubMed1998

A high-pressure, high-resolution NMR probe for experiments at 500 MHz.

A novel high-pressure, high-resolution NMR probe is described which operates at a frequency of 500 MHz. The design features an alternative RF coil (8 mm sample tube) for high frequency, sensitivity, probe power, and resolution (< 3.0 x 10(-9)). The probe is capable of pressures to at least 5 kbar over a temperature range of -30 to 80 degreesC, and has a double-tuned 1H/2H circuit which can tune at 1H frequencies of either 300 or 500 MHz. The sensitivity of the 300-MHz circuit is over twice that of previous 10-mm high-pressure NMR probe designs, while at 500 MHz the sensitivity is nearly five times that of previous 300-MHz pressure probes. Potential biochemical applications are demonstrated by 2D NOESY spectra of a Troponin C mutant.

Deuterium↗
PubMed1998

Metaphase fragility of the human RNU1 and RNU2 loci is induced by actinomycin D through a p53-dependent pathway.

Infection of human cells with adenovirus 12 (Ad12), but not Ad2 or 5, induces four specific sites of metaphase chromosome fragility: the U1 small nuclear RNA (snRNA) genes (the RNU1 locus), the U2 snRNA genes (RNU2), the U1 snRNA pseudogenes (PSU1) and the 5S rRNA genes (RN5S). Significantly, each of these sites corresponds to a multigene family encoding a small, abundant structural RNA. We and others have shown previously that Ad12-induced fragility of the RNU2 locus requires U2 snRNA promoter elements, viral early functions and p53 function, but not viral replication or integration, Rb function or chromosomal sequences flanking the RNU2 locus. Remarkably, we now find that very low doses of actinomycin D (5-50 ng/ml) can phenocopy Ad12 infection: metaphase fragility of the RNU1 and RNU2 loci is induced specifically in the absence of virus, and induction also requires U2 promoter elements and p53 function. Concurrently, it has been found by others that treatment with cytosine arabinoside (araC), but not aphidicolin, can also phenocopy Ad12 infection. We propose that Ad12 infection, actinomycin D and araC all induce a similar or identical global damage arrest signal (perhaps a modification or altered conformation of p53) that preferentially interferes with metaphase condensation of the RNU1 and RNU2 loci. The RNU1 and RNU2 loci could be especially sensitive to this global signal either because specialized U snRNA transcription factors interact uniquely with the signal, or because the high concentration of short, active transcription units hinders chromatin condensation.

Chromosome Fragility↗
PubMed1998

Adenovirus type 12-induced fragility of the human RNU2 locus requires p53 function.

Adenovirus type 12 (Ad12) infection of human cells induces four chromosomal fragile sites corresponding to the U1 small nuclear RNA (snRNA) genes (the RNU1 locus), the U2 snRNA genes (RNU2), the U1 snRNA pseudogenes (PSU1), and the 5S rRNA genes (RN5S). Ad12-induced fragility of the RNU2 locus requires U2 snRNA transcriptional regulatory elements and viral early functions but not viral replication or integration, or chromosomal sequences flanking the RNU2 locus. We now show that Ad12 cannot induce the RNU1, RNU2, or PSU1 fragile sites in Saos-2 cells lacking the p53 and retinoblastoma (Rb) proteins but that viral induction of fragility is rescued in these cells when the expression of wild-type p53 or selected hot-spot mutants (i.e., V143A, R175H, R248W, and R273H) is restored by transient expression or stable retroviral transduction. We also observed weak constitutive fragility of the RNU1 and RNU2 loci in cells belonging to xeroderma pigmentosum complementation groups B and D (XPB and XPD) which are partially defective in the ERCC2 (XPD) and ERCC3 (XPB) helicase activities shared between the repairosome and the RNA polymerase H basal transcription factor TFIIH. We propose a model for Ad12-induced chromosome fragility in which interaction of p53 with the Ad12 E1B 55-kDa transforming protein (and possibly E4orf6) induces a p53 gain of function which ultimately perturbs the RNA polymerase II basal transcription apparatus. The p53 gain of function could interfere with chromatin condensation either by blocking mitotic shutdown of U1 and U2 snRNA transcription or by phenocopying global or local DNA damage. Specific fragilization of the RNU1, RNU2, and PSU1 loci could reflect the unusually high local concentration of strong transcription units or the specialized nature of the U1 and U2 snRNA transcription apparatus.

Adenoviruses, Human↗
PubMed1998

[Microsurgical treatment of ischemic necrosis of the head of the 2nd metatarsal bone].

In order to explore a new method to treat the ischemic necrosis of the head of 2nd metatarsal bone in adult, transposition of reversed vascularized metatarsal bone graft was adopted in the treatment of 4 cases, 2 of which were followed up for one and a half years. The postoperative X-ray showed the round head of the 2nd metatarsal bone became round and even density. The clinical observation showed that there was excellent function of metatarsophalangeal joint. It was concluded that the reversed vascularized metatarsal bone graft could provide a reliable blood supply and various osteogenic factors to the avascularized head of the metatarsal bone, and the operation could also debride the joint cavity and carry out decompression.

Adult↗
PubMed1998

[Study on EEG signals data compression and spikes recognition with wavelet neural network].

A novel method of EEG signals compression representation and epileptiform spikes recognition based on wavelet neural network and its algorithm is presented in this paper. Wavelet network not only can compress data effectively but also can recover original signal. In addition the characteristics of the spikes and the spike-slow rhythm are detected automatically from the time-frequency isoline of EEG signal. This method can be generalized in the field of the electrophysiological signal processing and time-frequency analyzing.

Electroencephalography↗
PubMed1998

Probable ceftiofur-induced cutaneous drug reaction in a cow.

A cow with pyelonephritis was treated with ceftiofur (3 mg/kg body weight, IV, q12 h). Hair loss and pruritus were observed after 8 and 12 d of treatment, respectively. Ancillary laboratory tests supported a diagnosis of allergic disease. Clinical signs and laboratory test results normalized after ceftiofur administration was stopped.

Alopecia↗
PubMed1997

Developmental disorder associated with increased cellular nucleotidase activity.

Four unrelated patients are described with a syndrome that included developmental delay, seizures, ataxia, recurrent infections, severe language deficit, and an unusual behavioral phenotype characterized by hyperactivity, short attention span, and poor social interaction. These manifestations appeared within the first few years of life. Each patient displayed abnormalities on EEG. No unusual metabolites were found in plasma or urine, and metabolic testing was normal except for persistent hypouricosuria. Investigation of purine and pyrimidine metabolism in cultured fibroblasts derived from these patients showed normal incorporation of purine bases into nucleotides but decreased incorporation of uridine. De novo synthesis of purines and cellular phosphoribosyl pyrophosphate content also were moderately decreased. The distribution of incorporated purines and pyrimidines did not reveal a pattern suggestive of a deficient enzyme activity. Assay of individual enzymes in fibroblast lysates showed no deficiencies. However, the activity of cytosolic 5'-nucleotidase was elevated 6- to 10-fold. Based on the possibility that the observed increased catabolic activity and decreased pyrimidine salvage might be causing a deficiency of pyrimidine nucleotides, the patients were treated with oral pyrimidine nucleoside or nucleotide compounds. All patients showed remarkable improvement in speech and behavior as well as decreased seizure activity and frequency of infections. A double-blind placebo trial was undertaken to ascertain the efficacy of this supplementation regimen. Upon replacement of the supplements with placebo, all patients showed rapid regression to their pretreatment states. These observations suggest that increased nucleotide catabolism is related to the symptoms of these patients, and that the effects of this increased catabolism are reversed by administration of uridine.

5'-Nucleotidase↗
PubMed1997

Overexpression of metallothionein in the heart of transgenic mice suppresses doxorubicin cardiotoxicity.

Metallothionein (MT) may provide protection against doxorubicin-induced heart damage. To test this hypothesis, a heart-specific promoter was used to drive the expression of human MT-IIa gene in transgenic mice. Four healthy transgenic mouse lines were produced. Cardiac MT was constitutively overexpressed from 10- to 130-fold higher than normal. The MT concentration was not altered in liver, kidneys, lungs, or skeletal muscles. Other antioxidant components including glutathione, glutathione peroxidase, glutathione reductase, catalase, and superoxide dismutase were not altered in the MT-overexpressing heart. Mice (7-wk-old) from transgenic lines expressing MT activity 10- or 130-fold higher than normal and from nontransgenic controls were treated intraperitoneally with doxorubicin at a single dose of 20 mg/kg, and were killed on the 4th day after treatment. As compared to normal controls, transgenic mice exhibited a significant resistance to in vivo doxorubicin-induced cardiac morphological changes, and the increase in serum creatine phosphokinase activity. Atria isolated from transgenic mice and treated with doxorubicin in tissue bath was also more resistant to functional damage induced by this drug. The results provide direct evidence for the role of MT in cardioprotection against doxorubicin toxicity.

Animals↗
PubMed1997

At physiological pH, d(CCG)15 forms a hairpin containing protonated cytosines and a distorted helix.

To investigate potential structures of d(CGG/CCG)n that might relate to their biological function and association with triplet repeat expansion diseases (TREDs), the structure of a single-stranded (ss) oligonucleotide containing d(CCG)15 [ss(CCG)15] was examined by studies of the pH and temperature dependence of electrophoretic mobility, UV absorbance, circular dichroism, chemical modification, and P1 nuclease digestion. ss(CCG)15 had an unusually high pKa (7.7 +/- 0.2). At pH 8.5, ss(CCG)15 formed a relatively unstable (Tm = 30 degrees C in 1 mM Na+) hairpin containing CpG base-pair steps. At pH 7.5, the hairpin contained protonated cytosines but no detectable C x +C base pairs, increased thermal stability (Tm = 37 degrees C), increased stacking of the CpG base-pair steps, and a single cytosine that was flipped away from the central portion of the helix. Examination of ss(CCG)18 and ss(CCG)20, which were designed to adopt hairpins containing alternative GpC base-pair steps, revealed hairpins containing CpG base-pair steps, pKas of approximately 8.2 and approximately 8.4, respectively, and distorted helices. The results suggest that DNA sequences containing (CCG)(n > or = 15) adopt hairpin conformations that contain CpG rather than GpC base-pair steps; the mismatched cytosines are protonated at physiological pH but are not H-bonded. We propose that protonation arises from the stacking of two cytosines in the minor groove of a distorted helix.

Base Sequence↗
PubMed1997

Genetic staging of unresectable or metastatic neuroblastoma in infants: a Pediatric Oncology Group study.

BACKGROUND: Current staging systems for unresectable or metastatic neuroblastoma do not reliably predict responses to chemotherapy in infants under 1 year of age. Previous studies have indicated that the DNA content, or ploidy, of malignant neuroblasts can discriminate between good and poor responders in this group of patients, but the clinical utility of ploidy assessment has remained in question. PURPOSE: We tested, in a prospective nonrandomized study, the hypothesis that neuroblast ploidy could be used as the sole guide for treatment selection in infants with unresectable or metastatic tumors and could differentiate between those who would respond to our previous standard regimen and those who would benefit from an immediate switch to another therapy. METHODS: One hundred seventy-seven infants were enrolled in this trial. Five of these infants were subsequently excluded (two ineligible, two lacking ploidy information, and one protocol violation); therefore, 172 patients were included in the study. One hundred thirty infants with hyperdiploid tumors (DNA index > 1.0; better prognosis in retrospective studies) were treated with a well-tolerated regimen of cyclophosphamide (150 mg/m2 per day orally or intravenously on days 1-7) and doxorubicin (35 mg/m2 intravenously on day 8). Forty-two infants with diploid tumors (DNA index = 1.0; worse prognosis in retrospective studies) received cisplatin (90 mg/m2 intravenously on day 1) and teniposide (100 mg/ m2 intravenously on day 3) after an initial course of cyclophosphamide plus doxorubicin. Statistical end points were response and long-term survival. In addition, we assessed within each ploidy group (i.e., patients with hyperdiploid tumors and those with diploid tumors) the prognostic significance of NMYC gene copy number, tumor stage, and other variables commonly measured in this disease. RESULTS: Of the 127 assessable infants with hyperdiploid tumors, 115 (91%) had complete responses--85 after receiving five courses of cyclophosphamide plus doxorubicin and 30 after receiving further therapy including cisplatin plus teniposide. The 3-year survival estimate for the entire hyperdiploid group was 94% (95% confidence interval [CI] = 89%-98%). Nineteen (46%) of 41 assessable infants with diploid tumors were complete responders. The overall 3-year survival estimate for this group was 55% (95% CI = 39%-70%). Prognostic factor analysis indicated that NMYC gene amplification and an elevated serum lactate dehydrogenase level were statistically significant markers of higher risk disease within the diploid group (two-sided P values of .005 and .003, respectively). Only NMYC was predictive in the hyperdiploid group (P = .003). CONCLUSION: Use of a prognostic staging system based on tumor cell ploidy, augmented with the NMYC gene copy number and serum level of lactate dehydrogenase, would very likely improve the treatment of infants with unresectable or metastatic neuroblastoma. Patients with diploid tumors characterized by an amplified NMYC locus represent a particularly unfavorable risk group that may benefit from innovative new therapies.

Antibiotics, Antineoplastic↗
PubMed1997

Frequent inactivation of the p16 gene in human pituitary tumors by gene methylation.

Rodent models of pituitary tumorigenesis have implicated the retinoblastoma (Rb) pathway in the development of pituitary tumors. Previously, we reported that loss of p16 expression rather than loss of Rb occurs in most human pituitary adenomas. This alteration in these tumors is not associated with p16 mutation or frequent homozygous p16 gene loss. Our laboratory has now demonstrated that in most human pituitary tumors, the 5' CpG island of the p16 gene is extensively methylated. The high frequency of p16 gene methylation in human pituitary tumors suggests that this alteration is an early and perhaps required event in pituitary cell transformation.

Adenoma↗
PubMed1997

Structural and functional analysis of hypoxia-inducible factor 1.

Hypoxia-inducible factor 1 (HIF-1) is a basic helix-loop-helix protein that activates transcription of hypoxia-inducible genes, including those encoding: erythropoietin, vascular endothelial growth factor, heme oxygenase-1, inducible nitric oxide synthase, and the glycolytic enzymes aldolase A, enolase 1, lactate dehydrogenase A, phosphofructokinase I, and phosphoglycerate kinase 1. Hypoxia response elements from these genes consist of a HIF-1 binding site (that contains the core sequence 5'-CGTG-3') as well as additional DNA sequences that are required for function, which in some elements include a second HIF-1 binding site. HIF-1 is a heterodimer. The HIF-1 alpha subunit is unique to HIF-1, whereas HIF-1 beta (ARNT) can dimerize with other bHLH-PAS proteins. Structural analysis of HIF-1 alpha revealed that dimerization with HIF-1 beta (ARNT) requires the HLH and PAS domains, DNA binding is mediated by the basic domain, and that HIF-1 alpha contains a carboxyl-terminal transactivation domain. Co-transfection of HIF-1 alpha and HIF-1 beta (ARNT) expression vectors and a reporter gene containing a wild-type hypoxia response element resulted in increased transcription in non-hypoxic cells and a superinduction of transcription in hypoxic cells, whereas HIF-1 expression vectors had no effect on the transcription of reporter genes containing a mutation in the HIF-1 binding site. HIF-1 alpha and HIF-1 beta (ARNT) protein levels were induced by hypoxia in all primary and transformed cell lines examined. In HeLa cells, the levels of HIF-1 alpha and HIF-1 beta protein and HIF-1 DNA-binding activity increased exponentially as cellular oxygen tension decreased, with maximum values at 0.5% oxygen and half-maximal values at 1.5 to 2% oxygen. HIF-1 alpha and HIF-1 beta (ARNT) mRNAs were detected in all human, mouse, and rat organs assayed and mRNA expression was modestly induced in rodents subjected to hypoxia. HIF-1 alpha protein levels were induced in vivo when animals were subjected to anemia or hypoxia. The HIF1A gene was mapped to human chromosome 14q21-q24 and mouse chromosome 12.

Animals↗
PubMed1997

Lack of degeneration of loci on the neo-Y chromosome of Drosophila americana americana.

The extent of genetic degeneration of the neo-Y chromosome of Drosophila americana americana has been investigated. Three loci, coding for the enzymes enolase, phosphoglycerate kinase and alcohol dehydrogenase, have been localized to chromosome 4 of D. a. americana, which forms the neo-Y and neo-X chromosomes. Crosses between D.a. americana and D. virilis or D. montana showed that the loci coding for these enzymes carry active alleles on the neo-Y chromosome in all wild-derived strains of americana that were tested. Intercrosses between a genetically marked stock of virilis and strains of americana were carried out, creating F3 males that were homozygous for sections of the neo-Y chromosome. The sex ratios in the F3 generation of the intercrosses showed that no lethal alleles have accumulated on any of the neo-Y chromosomes tested. There was evidence for more minor reductions in fitness, but this seems to be mainly caused by deleterious alleles that are specific to each strain. A similar picture was provided by examination of the segregation ratios of two marker genes among the F3 progeny. Overall, the data suggest that the neo-Y chromosome has undergone very little degeneration, certainly not to the extent of having lost the functions of vital genes. This is consistent with the recent origin of the neo-Y and neo-X chromosomes, and the slow rates at which the forces that cause Y chromosome degeneration are likely to work.

Animals↗