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Biomedical subjects

P Liu

Publications and source records attributed to P Liu.

At least 325 records · Page 18Linked to original sources
PubMed1994

Priming of phagocytes for reactive oxygen production during hepatic ischemia-reperfusion potentiates the susceptibility for endotoxin-induced liver injury.

Plasma levels of glutathione disulfide (GSSG) as an indicator of a vascular oxidant stress, tumor necrosis factor-alpha (TNF-alpha) formation, and liver injury (alanine aminotransferase activity, histology) were monitored in male Fischer rats after 30 min of hepatic ischemia followed by up to 4 hr of reperfusion. The injection of 1 mg/kg Salmonella enteritidis endotoxin at 30 min of reflow potentiated the postischemic oxidant stress and liver injury. TNF-alpha levels increased from 10 +/- 7 pg/ml (baseline) to 3,553 +/- 738 pg/ml after ischemia-reperfusion followed by endotoxin, or to 3,670 +/- 508 pg/ml after endotoxin alone. Depletion of serum complement before ischemia attenuated the endotoxin-mediated increase of reactive oxygen formation by 70% but did not affect TNF-alpha levels. Complement activation with cobra venom factor (CVF) during reperfusion had an effect similar to that of endotoxin on the oxidant stress and liver injury. CVF did not increase TNF-alpha formation during reperfusion. Kupffer cells and neutrophils isolated from the postischemic liver 2.5 hr after endotoxin injection generated 600% and 400% more superoxide, respectively, than cells isolated from control livers. The results demonstrate a substantial priming of hepatic phagocytes for reactive oxygen production but not TNF-alpha formation, even after short periods of hepatic ischemia, and the vulnerability of the postischemic liver to severe endotoxin-induced injury. Activated complement seems to be mainly responsible for the effects. These results may explain the high risk for hepatic failure after extensive liver resection and hypovolemic shock.

Adenosine Triphosphate↗
PubMed1994

[Chromosomal analysis of human eggs fertilized in vitro].

With the advent of IVF-ET, human oocytes and early embryos are now available for chromosomal analysis. In this study, 44 chromosomal preparations of human oocytes or early embryos from 36 women in an IVF program were analyzed. 13 oocytes with normal haploid chromosome complement were not fertilized. The cause of failure of fertilization was attributed to either male factors or to immaturity of oocytes. 4 oocytes not fertilized were found to be either hyperhaploid or hypohaploid. Among 26 fertilized but not cleavaged oocytes 8 were also abnormal, 7 were normal haploid but in different developmental stages with the fertilizing sperms, 11 showed polyspermia. One two-cell embryo showed normal diploid set. The high ratio of oocyte chromosomal abnormalities and abnormal fertilization may be explained by the use of drug hyperstimulation of follicular development. Similar abnormalities, although to a lesser extent, may occur in a natural reproductive process.

Adult↗
PubMed1994

[The observation of therapy of anemia in chronic renal failure with recombinant human erythropoietin].

Anemia is one of the serious complications of chronic renal failure, therapy with recombinant human erythropoietin (r-HuEPO) can correct such anemia officiently. For most patients, the initial dose of r-HuEPO is 100U/kg, by intravenously or subcutaneous, three times a week. After 6 weeks of treatment, Hb could increase to 100g/L, and Hct to above 0.33-0.35. Then 500/kg 3 time a week can be used as maintaining dose. 4 patients need maintaining dose of 150U/kg, for pulmonary infection, poor nutrition, and poor iron supply. Therefore, during the treatment, iron folie acid and Vit B12 should be applied sufficiently and treat the infection effectively with the increasing of Hb and Hct, 2/3 of the patients have hypertension which can be controlled with medication. If there is thrombosis in the dialyzer, the dose of heparin should be increased. The patients on r-HuEPO should be dialysised sufficiently to prevent hyperkalemia.

Adult↗
PubMed1994

Results of left ventricular aneurysmectomy with a tailored scar excision and primary closure technique.

Controversy exists concerning which surgical technique is optimal for ventricular aneurysm repair. In 92 (97%) of 95 patients, we tailored scar excision to remove nonfunctioning wall and restore left ventricular geometry and shape toward normal while allowing linear closure. Preoperative and/or postoperative multiple gated acquisition scans were obtained in 76 (83%) of 92 patients and Doppler echocardiograms in 79 (86%) of 92. Before operation 78 patients (85%) were in New York Heart Association class III or IV with congestive heart failure in 58 (63%), angina in 69 (75%) and syncope in 46 (50%) of the 92 patients. Additional operative procedures included aorta-coronary bypass grafting in 81 patients (88%), septoplasty in 4 (4%), and arrhythmia ablation in 54 (59%). Hospital mortality was 3 (3%) of 92 patients. There have been 15 late deaths caused by congestive heart failure with or without mitral regurgitation (7 of 15). Among survivors 66 (89%) of 74 were symptomatically improved with 25 (34%) of 74 in New York Heart Association class I, 24 (32%) of 74 in class II, 19 (26%) of 74 in class III, and 6 (8%) of 74 in class IV. Actuarial survival was 88%, 86%, and 80% at 1, 2, and 5 years, respectively, and was not different for patients with a preoperative left ventricular ejection fraction less than 20%. In 47 patients with an anterior aneurysm who had preoperative and postoperative studies, multiple gated acquisition scans showed improvement in left ventricular ejection fraction from 23% to 30% (p < 0.001). Preoperative Doppler echocardiograms showed significant mitral regurgitation (2+ or more) in 26 (36%) of 72 patients studied. Of these, 21 had postoperative studies and mitral regurgitation was improved by at least one grade in 12 (57%) of 21 patients. We conclude that aneurysm repair with a tailored scar excision and linear closure is associated with low operative mortality, objective evidence of improvement in left ventricular function, symptomatic relief, and long-term survival even in patients with advanced left ventricular dysfunction and mitral regurgitation.

Echocardiography, Doppler↗
PubMed1994

Effects of oxygen free radicals and scavengers on the cardiac extracellular collagen matrix during ischemia-reperfusion.

OBJECTIVE: Collagen is lysed early during ischemia-reperfusion, but whether this is due to ischemia or reperfusion injury is not known. The effect of oxygen free radicals and free radical scavengers on left ventricular hemodynamics, myocardial morphology and collagen content were studied in an isolated, Langendorff-perfused rat heart model of regional ischemia-reperfusion. METHODS: All hearts received left anterior descending coronary artery ischemia for 20 mins. Group 1 had ischemia only; group 2 had ischemia followed by reperfusion with oxygenated Krebs-Henseleit buffer for 20 mins; group 3 had oxygen free radicals generated by hypoxanthine and xanthine oxidase during reperfusion; group 4 had free radical scavengers with superoxide dismutase plus catalase; group 5 had both oxygen free radicals and free radical scavengers during reperfusion. RESULTS: Left ventricular developed pressure decreased significantly in group 3 during ischemia followed by reperfusion (58 +/- 3.1 mmHg versus 42 +/- 2.4 mmHg, P = 0.004), but did not change significantly in any of the other groups. Necrosis score on pathology was highest in group 3; this score also was higher than that in group 5 with free radical scavengers added (3.0 +/- 0.3 versus 2.0 +/- 0.4, P = 0.07) and higher than that of group 2 with reperfusion with buffer only (3.0 +/- 0.3 versus 1.4 +/- 0.5, P < 0.05). Collagen content decreased significantly compared with control in group 3 only with ischemia followed by reperfusion with the addition of oxygen free radicals (18.4 +/- 1.5 versus 11.9 +/- 1.7 g/mg protein, P < 0.05). The addition of free radical scavengers in group 5 mainly attenuated the collagen loss. Scanning electron microscopy revealed profound structural changes of the extracellular collagen matrix in numerous regions of 'stunning' independent of tissue necrosis. CONCLUSIONS: We conclude that: first, oxygen free radicals trigger significant collagen damage and left ventricular dysfunction during reperfusion; second, these changes extend beyond the ischemic damage alone; and third, free radical scavengers can effectively limit oxygen free radical-induced collagen loss and left ventricular dysfunction.

Animals↗
PubMed1994

Central blood volume in cirrhosis: measurement with radionuclide angiography.

In patients with cirrhosis a diminished effective central arterial blood volume associated with systemic arterial vasodilation has been proposed as the mechanism that initiates renal sodium retention. Furthermore, total central blood volume has recently been reported as reduced in cirrhosis, and the controversy over the stimulus for sodium retention in cirrhosis remains. The aim of this study was to assess the central blood volume with radionuclide angiography to determine whether there is effective arterial underfilling in cirrhosis. Twenty-nine patients (13 with and 16 without ascites) and 10 age- and sex-matched control subjects were studied under metabolic conditions. Radionuclide ventricular volume and total central blood volume were determined from gated images, taking into account the 99Tc count activity per milliliter of blood volume and attenuation. The pulmonary volumes were similarly derived.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Fusion between transcription factor CBF beta/PEBP2 beta and a myosin heavy chain in acute myeloid leukemia.

The pericentric inversion of chromosome 16 [inv(16)(p13q22)] is a characteristic karyotypic abnormality associated with acute myeloid leukemia, most commonly of the M4Eo subtype. The 16p and 16q breakpoints were pinpointed by yeast artificial chromosome and cosmid cloning, and the two genes involved in this inversion were identified. On 16q the inversion occurred near the end of the coding region for CBF beta, also known as PEBP2 beta, a subunit of a heterodimeric transcription factor regulating genes expressed in T cells; on 16p a smooth muscle myosin heavy chain (SMMHC) gene (MYH11) was interrupted. In six of six inv(16) patient samples tested, an in-frame fusion messenger RNA was demonstrated that connected the first 165 amino acids of CBF beta with the tail region of SMMHC. The repeated coiled coil of SMMHC may result in dimerization of the CBF beta fusion protein, which in turn would lead to alterations in transcriptional regulation and contribute to leukemic transformation.

Amino Acid Sequence↗
PubMed1993

Identification of yeast artificial chromosomes containing the inversion 16 p-arm breakpoint associated with acute myelomonocytic leukemia.

We report the cloning of the chromosome 16 p-arm breakpoint involved in inversion 16(p13;q22) associated with subtype of acute myelomonocytic leukemia (AMML) M4Eo. Inter-Alu polymerase chain reaction (PCR) products from a series of interspecific somatic cell hybrids that contain only small portions of the human chromosome 16 p-arm were generated for use as fluorescent in-situ hybridization (FISH) probes. When applied to patient cells, rapid and unambiguous identification of the inversion resulted. Using FISH analysis, cosmid clones associated with the hybrids were identified that bracketed the p-arm breakpoint. A repeat-free fragment of one of these cosmids (35B11) when used as probe on Southern blots from pulsed-field gels identified rearranged macrorestriction fragments in patient DNA. Yeast artificial chromosomes (YACs) were isolated using sequences derived from cosmids flanking 35B11 in a cosmid contig. Of 4 YACs so identified, 3 were shown by FISH to cross the inversion-16 p-arm breakpoint. Therefore, the breakpoint has been molecularly cloned, and identified as being within these 3 YACs. These clones will facilitate the unraveling of the genetic events associated with inversion-16 and are available tools with immediate clinical application.

Base Sequence↗
PubMed1993

Activation of phospholipase A2 and stimulation of prostaglandin E2 production by transforming growth factor-alpha in rat thymic epithelial cells requires influx of calcium.

The stimulation of both phospholipase A2 (PLA2) enzymic activity and the production of prostaglandin E2 (PGE2) by transforming growth factor-alpha (TGF-alpha) and Ca2+ ionophore A23187 in TEA3A1 rat thymic epithelial cells were studied. TGF-alpha by itself at various concentrations (5-200 ng/ml) had no effect on the stimulation of PGE2 production. A23187 (1 microgram/ml) by itself stimulated PGE2 production on average by 18-fold over the control. When TGF-alpha (50 ng/ml) was added to the cells in the presence of A23187, a synergistic stimulation (on average 45-fold) of PGE2 production was observed. Synergistic stimulation was also observed at the level of arachidonic acid released from phospholipid pools, suggesting the activation of PLA2 enzymic activity. We have found that this synergistic activation of PLA2 enzymic activity and subsequent stimulation of PGE2 production required the activation of epidermal growth factor (EGF) receptor tyrosine kinase and Ca2+ influx. This was shown by the fact that genistein, an inhibitor of tyrosine kinase, blocks the synergistic stimulation by TGF-alpha and A23187 and by the fact that the stimulation of PGE2 production by TGF-alpha and A23187 is dependent on the culture-medium Ca2+ concentrations. The requirement for Ca2+ influx instead of intracellular mobilization of Ca2+ was shown by the fact that PGE2 production was not stimulated when cells were treated with TGF-alpha and thapsigargin. Moreover, the synergistic stimulation of PGE2 production by TGF-alpha and A23187 was not affected in protein kinase C down-modulated cells. In addition, the synergistic stimulation was not observed in cells treated with either phorbol 12-myristate 13-acetate (PMA) and TGF-alpha or PMA and A23187, and in cells treated with TGF-alpha and thapsigargin. The requirement for the activation of receptor tyrosine kinase seems to be specific to the EGF receptor, since a synergistic stimulation of PGE2 production was not observed when cells are treated with either insulin-like growth factor-I or fibroblast growth factor-I in the presence of A23187.

Animals↗
PubMed1993

Smooth muscle myosin heavy chain locus (MYH11) maps to 16p13.13-p13.12 and establishes a new region of conserved synteny between human 16p and mouse 16.

The human smooth muscle myosin heavy chain locus (MYH11) was mapped by fluorescence in situ hybridization to the middle of the p arm of chromosome 16 using a genomic cosmid clone containing coding sequences of the gene as probe. Probe from coding sequence, when applied to Southern blots of a panel of hybrids containing different portions of human chromosome 16, localized the gene to 16p13.13-13.12. Coding sequence PCR primers, when used on the DNA from a CHO-mouse hybrid clone mapping panel informative for mouse chromosomes, showed that the gene was located on mouse chromosome 16. These results correct a recent assignment of MYH11 from 16q12.2 to the region of the 16p-arm inversion breakpoint seen in acute myelomonocytic leukemia (AMML) M4Eo and demonstrate that the conflicting data do not result from the presence of additional MYH genes on the q arm of the chromosome. Also, a new region of conserved synteny between human 16p and mouse 16 is established.

Animals↗
PubMed1993

Sonographic appearance of Sertoli cell tumour: with pathologic correlation.

Sertoli cell tumor is a rare tumor of the testis, with a good prognosis following orchiectomy in the pediatric patient. Sonography of such a tumor in a 5-year-old boy revealed diffuse inhomogeneous increase in echogenicity in an enlarged left testicle. The increased echogenicity of the testicle reflected the dense collagenous matrix of the lesion.

Child, Preschool↗
PubMed1993

Dual Alu polymerase chain reaction primers and conditions for isolation of human chromosome painting probes from hybrid cells.

A method for rapid and efficient production of chromosome- and chromosome-region specific probes for fluorescent in situ hybridization (FISH) detectable by simple fluorescent microscopy is described. The procedure is based on simultaneous use of two inter-Alu-polymerase chain reaction (PCR) primers for extraction of highly heterogeneous human DNA from interspecific somatic cell hybrids containing the chromosome regions of interest. Probes so produced do not hybridize to centromeric sequences and simultaneously band the target chromosomes, making them useful for unambiguous identification of chromosomal elements and breakpoints associated with cancer.

Animals↗
PubMed1993

Viral myocarditis: a paradigm for understanding the pathogenesis and treatment of dilated cardiomyopathy.

Although an etiologic link between viral myocarditis and idiopathic dilated cardiomyopathy has long been recognized, the actual extent of this relation has been uncertain. In this review, we examine recent developments in the molecular analysis of endomyocardial biopsy specimens, particularly techniques for gene amplification, which have unequivocally confirmed this relation and given us some insight into its significance. In addition, we show that viral myocarditis in a murine model is associated with spasm of the coronary microvasculature, leading to myocyte necrosis, fibrosis, calcification and cardiac dilation. These findings are similar to those seen in the hearts of genetically cardiomyopathic hamsters, rats and humans with hypertension and diabetes, rats after acute brain injury and models of Chagas' disease. Treatment of microvascular spasm with verapamil, captopril or alpha 1-adrenergic blocking agents appears to interrupt this pathway and has been shown to markedly impede the evolution of dilated cardiomyopathy in the genetic hamster model and a murine model of myocarditis. There is some suggestion that digitalis, though beneficial during cardiac decompensation, may actually be detrimental when administered during the early stages of myocardial disease. These experiments have led to a new paradigm for the pathogenesis of cardiomyopathy after viral myocarditis, as well as a general hypothesis for the pathogenesis of some types of dilated cardiomyopathy. They also suggest that the selection of therapeutic agents for some forms of dilated cardiomyopathy may differ significantly between the early and late stages of the disease.

Animals↗
PubMed1993

Flow-through system effects on in vitro analysis of transdermal systems.

The development of transdermal therapeutic systems (TTS) often involves in vitro evaluation of formulations and prototypes using flow-through diffusion cells. The apparent flux obtained from such methodologies does not accurately represent the actual (intrinsic) permeation of the compound through the skin. Flow-through system parameters, i.e., fraction collector tube volume, receiver cell volume, flow rate, and sampling interval, modify the flux yielding an apparent flux. Both finite-dose flux profiles and infinite-dose diffusional lag times are modified by these parameters. In this study, a transfer function is derived which describes the effect of these parameters. The intrinsic flux is calculated from apparent flux data using the transfer function and experimental flow-through system parameters. This allows the calculation of permeant flux profiles devoid of modification by the experimental methodology.

Administration, Cutaneous↗
PubMed1993

Regional mapping of human DNA excision repair gene ERCC4 to chromosome 16p13.13-p13.2.

Mitomycin C (MMC)-resistant interspecific somatic cell hybrids made between human cells and the MMC-sensitive, Chinese hamster ovary (CHO) excision repair-deficient UV41 cells generally contained human chromosome 16, while other human chromosomes were randomly present. MMC-sensitive and -resistant subclones were isolated from resistant clones, and resistance generally segregated concordantly with human chromosome 16 markers. UV radiation survival analysis of subclones indicated that MMC and UV resistance were correlated. Therefore, the complementing gene, Excision Repair Cross Complementing 4 (ERCC4), was assigned to human chromosome 16. Complementation of UV41 by human cells derived from patients with xeroderma pigmentosum groups A, C, D and F excluded ERCC4 from involvement in those disease syndromes. Resistant hybrids containing only portions of chromosome 16 were identified by the lack of concordance of multiple chromosome 16 markers. When such hybrids were used as a source of probe for fluorescent in situ hybridization onto normal human metaphases, the only region of chromosome 16 identified as being consistently present was 16p13.1-p13.3. Genetic marker analysis of informative hybrids with mapped probes refined the position of ERCC4 to 16p13.13-p13.2 and allowed the following order of markers within the region to be established: pter--(PRM1, D16S215)-D16S213-D16S53-(D16S214,ERCC4) -D16S3-D16S96-cen.

Animals↗