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Biomedical subjects

E Li

Publications and source records attributed to E Li.

At least 109 records · Page 6Linked to original sources

[Combined laparoscopic surgery].

With minimal and flexible access, combined laparoscopic surgery (CLS) is most suitable to treat several abdominal diseases simultaneously. Among 1000 cases of laparoscopic procedures since 1991, 52 were CLS. They were laparoscopic cholecystectomy (LC) + appendectomy (LA) 24, LC + laparoscopic fenestration of liver cyst (LFLC) 2, LC + laparoscopic herniorraphy (LH) 4, LC + laparoscopic common bile duct exploration (LCBDE) 12, LC + laparoscopic salpingo-ophorectomy 1, LC + laparoscopic removal of leiomyoma of uterus (LRLU) 1, LC + laparoscopic excision of hemangioleiomyolipoma (LEH) in right kidney 1, LH + laparoscopic varicocelectomy (LV) 2, laparoscopic paraesophageal hernia repair + nissen fundoplication 5. CLS was successfully performed laparoscopically without morbidity and mortality. One case of LC + LCBDE and one case of LH + LNF converted to open surgery be cause of unexpected injury of cystic artery and esophageal rupture. Compared with single laparoscopic surgery, CLS did not increase postoperative pain, hospitalization, recovery period, and cost for equipment and instruments. Our results showed that as long as we insist on basic surgical principles, strictly follow operative indications for CLS, more and more patients with multiple abdominal diseases will enjoy minimal access surgery.

Adult↗

[Effects of icarrin on secretive function of cultured granulosa and adrenal cortical cells of rats].

Icarrin was added to cultured cells and the hormones in culture fluid were determined after 3 hours of incubation. The results showed that icarrin (30-1000 micrograms/L) could promote the estradiol production of granulosa cells. The most effective concentration was 100 micrograms/L. Icarrin also exerted a stimulatory effect on corticosterone production at the highest dosage (1000 micrograms/L).

Adrenal Cortex↗

Hereditary angioedema in a Chinese family.

Hereditary angioedema is characterised by recurrent episodes of peri-orbital and peri-oral swelling which can cause an upper airway obstruction, abdominal pain, vomiting, diarrhoea, and even hypotensive collapse. This potentially fatal condition is frequently misdiagnosed; its early recognition and appropriate treatment are thus important. We report a familial cluster of hereditary angioedema in a Chinese family and describe the clinical course of two patients.

Journal Article↗

[Study on the stunted culture of trees of Scaphium lychnophorum].

Taking these cultural practices, grafting by the ingraftment of side branch on the place of flowering with the dwarf stock, tip pruning on time to make branches growing and rational pruning etc can make the trees of Scaphium lychnbophorum dwafing effectively. The stunted trees are only high 3-5 m and their branches are only high about 1 m from the ground. Some of them first flower until five years after they are cultivated.

Malvaceae↗

[A technique of PVC detection in QRS wave].

A technique of PVC detection is described in this paper. The procedures of PVC analysis include noise detection, QRS detection, feature extraction and QRS wave classification. The interference is detected in hierarchy ways. A new non-linear transformation of ECG waveform is given to be taken as the QRS detection function. Taking this QRS detection function, the influence of noise and interference can be reduced greatly. By the technique of QRS template matching, QRS waveforms are sorted into different clusters in QRS wave form space. Then a linear classifier is used to identify the medical meaning of these clustes. Before the linear classifier is applied, the QRS waveforms are classified according to some special decision rules. 38 half-hour standard database is used to test the technique presented in this paper. The result shows t hat accuracy rate of PVC detection is better than 95%.

Cluster Analysis↗

[Experimental study on free grafting of fat particles].

Forty-eight rats were used to study the change in fat tissue after grafting. In the experimental group, the fat tissue to be grafted was treated with insulin. Evaluation was made by graft measurement, ink injection, light microscopic and electronic microscopic observations. The results showed that the volume of the grafted fat decreased obviously and there was no significant difference between the experimental and the control groups in the change of volume of the grafted fat tissue. At the early stage of grafting, the grafted fat showed ischemia. The adipocytes released lipid and dedifferentiated to preadipocytes. After revascularization, the preadipocytes began to absorb lipid and became mature adipocytes. The structure of the grafted fat was almost normal at 6 months after grafting. The formation of the cytoskeletal filament, found by ultrastructural study, was closely related with the synthesis of lipid.

Abdominal Muscles↗

Provirus integration into a gene encoding a ubiquitin-conjugating enzyme results in a placental defect and embryonic lethality.

Ubiquitin-conjugating enzymes (E2 or Ubc) constitute a family of conserved proteins that play a key role in ubiquitin-dependent degradation of proteins in eukaryotes. We describe here a transgenic mouse strain where retrovirus integration into an Ubc gene, designated UbcM4, results in a recessive-lethal mutation. UbcM4 is the mouse homologue of the previously described human UbcH7 that is involved in the in vitro ubiquitination of several proteins including the tumor suppressor protein p53. The provirus is located in the first intron of the gene. When both alleles are mutated the level of steady-state mRNA is reduced by about 70%. About a third of homozygous mutant embryos die around day 11.5 of gestation. Embryos that survive that stage are growth retarded and die perinatally. The lethal phenotype is most likely caused by impairment of placenta development as this is the only organ that consistently showed pathological defects. The placental labyrinth is drastically reduced in size and vascularization is disturbed. The UbcM4 mouse mutant represents the first example in mammals of a mutation in a gene involved in ubiquitin conjugation. Its recessive-lethal phenotype demonstrates that the ubiquitin system plays an essential role during mouse development.

Alleles↗

Complete phenotypic characterization of apobec-1 knockout mice with a wild-type genetic background and a human apolipoprotein B transgenic background, and restoration of apolipoprotein B mRNA editing by somatic gene transfer of Apobec-1.

We have produced gene knockout mice by targeted disruption of the apobec-1 gene. As recently reported by Hirano et al. (Hirano, K.-I., Young, S. G., Farese, R. V., Jr., Ng, J., Sande, E., Warburton, C., Powell-Braxton, L. M., and Davidson, N. O. (1996) J. Biol. Chem. 271, 9887-9890), these animals do not edit apolipoprotein (apo) B mRNA or produce apoB-48. In this study we have performed a detailed analysis of the lipoprotein phenotypic effects of apobec-1 gene disruption that were not examined in the previous study. We first analyzed the plasma lipoproteins in knockout animals with a wild-type genetic background. Although there was no difference in plasma cholesterol between apobec-1(-/-), +/-, or +/+ mice, there was a marked (176%) increase in plasma apoB-100, from 1.8 +/- 1.2 mg/dl in apobec-1(+/+) mice to 2.7 +/- 0.6 mg/dl in apobec-1(+/-) and 5.0 +/- 1.4 mg/dl in apobec-1(-/-) mice. Plasma apoE was similar in these animals. By fast protein liquid chromatography (FPLC) analysis, there was a significant decrease in plasma high density lipoprotein (HDL) cholesterol in apobec-1(-/-) mice. We further fractionated the plasma lipoproteins into d < 1.006, 1.006-1.02, 1.02-1.05, 1.05-1.08, 1.08-1.10, and 1.10-1.21 g/ml classes, and found a marked (30-40%) reduction in the cholesterol and protein content in the (d 1.08-1.10 and 1.10-1.21) HDL fractions, corroborating the FPLC data. SDS-gel analysis revealed an absence of apoB-48, an increase in apoB-100 in the very low density lipoprotein (VLDL) and low density lipoprotein (LDL) fractions, and a small decrease in apoA-I in the HDL fractions in the apobec-1(-/-) samples. We next raised the basal plasma apoB levels in the apobec-1(-/-) animals by cross-breeding them with human apoB transgenic (TgB) mice. The plasma apoB-100 was 3-fold higher in apobec-1(-/-)/TgB+/- mice (26.6 +/- 18.3 mg/dl) than in apobec-1(+/+)/TgB+/- mice (9.8 +/- 3.9 mg/dl, p < 0.05). The apobec-1(-/-)/TgB+/- mice had a plasma cholesterol levels of 170 +/- 28 mg/dl and triglyceride levels of 106 +/- 31 mg/dl, which are 80% and 58% higher, respectively, than the corresponding values of 94 +/- 21 mg/dl and 67 +/- 11 mg/dl in apobec+/+/TgB+/- mice. By FPLC, the apobec-1(-/-)/TgB+/- animals developed markedly elevated plasma LDL cholesterol (518.5 +/- 329.5 microg/ml) that is 373% that of apobec1(+/+)/TgB+/- mice (139.0 +/- 87.0 microg/ml) (p < 0.05). The elevated plasma triglyceride was accounted for mainly by a 97% increase in VLDL triglyceride in the apobec1(-/-)/TgB+/- mice. We conclude that apobec-1(-/-) animals have a distinctive lipoprotein phenotype characterized by significant hyperapoB-100 and HDL deficiency in mice with a wild-type genetic background. Furthermore, the abolition of apoB mRNA editing elevates plasma total cholesterol and LDL cholesterol in apobec-1(-/-) animals with a TgB background. Finally, to exclude the possibility that absence of apoB mRNA editing was a secondary effect of chronic Apobec-1 deficiency, we treated apobec-1(-/-) mice with a replication-defective mouse Apobec-1 adenoviral vector and found that we could acutely restore apoB mRNA editing in the liver. These experiments indicate that Apobec-1 is an essential component of the apoB mRNA editing machinery and absence of editing in the knockout animals is a direct consequence of the absence of functional Apobec-1.

APOBEC-1 Deaminase↗

Conformationally defined 6-s-trans-retinoic acid analogs. 3. Structure-activity relationships for nuclear receptor binding, transcriptional activity, and cancer chemopreventive activity.

We recently demonstrated that conformationally defined 6-s-trans-retinoic acid (RA) analogs were effective in the prevention of skin papillomas (Vaezi et al. J. Med. Chem. 1994, 37, 4499-4507) and selective agonists for nuclear receptor binding and activation (Alam et al. J. Med. Chem. 1995, 38, 2302-2310). In order to probe important structure-activity relationships, we evaluated a homologous series of four 6-s-trans-retinoids that are 8-(2'-cyclohexen-1'-ylidene)-3,7-dimethyl-2,4,6-octatrienoic acids with different substituents at 2' (R2) and 3' (R1) positions on the cyclohexene ring. UAB1 (R1 = R2 = H), UAB4 (R1 = R2 = Me), UAB7 (R1 = Me, R2 = iPr), and UAB8 (R1 = Et, R2 = iPr) contain alkyl R groups that mimic, to different extents, portions of the trimethylcyclohexenyl ring of RA. Both 9Z- and all-E-isomers of these retinoids were evaluated in binding assays for cellular retinoic acid-binding proteins (CRABP-I and CRABP-II), a nuclear retinoic acid receptor (RAR alpha), and a nuclear retinoid X receptor (RXR alpha). The all-E-isomers of UAB retinoids bound tightly to CRABPs and RAR alpha, the binding affinity of the all-E-isomer increased systematically from UAB1 to UAB8, and binding for the latter was comparable to that of all-E-RA. In contrast to RA, the (9Z)-UAB retinoids were at least 200-fold less active than the all-E-isomers in binding to RAR alpha. The (9Z)-UAB isomers exhibited increasingly stronger binding to RXR alpha, and (9Z)-UAB8 was nearly as effective as (9Z)-RA in binding affinity. The retinoids were also evaluated in gene expression assays mediated by RAR alpha and RXR alpha homodimers or RAR alpha/RXR alpha heterodimers. Consistent with the binding affinities, the (all-E)-UAB retinoids activated gene transciption mediated by RAR alpha homodimers or RAR alpha/RXR alpha heterodimers, while the (9Z)-UAB isomers activated only the RXR alpha homodimer-mediated transcription. The all-E- and 9Z-isomers of the UAB retinoids were further evaluated for their capacity to prevent the induction of mouse skin papillomas. When compared to RA, only the (all-E)-UAB retinoids containing bulky R1 and R2 groups were effective in this chemoprevention assay. (9Z)-RA displayed equal capacity as RA to prevent papillomas, while the 9Z-isomers of the UAB retinoids were much less effective. Taken together, these studies demonstrate that the cyclohexenyl ring substituents of 6-s-trans-UAB retinoids are important for their biological activities and that the chemopreventive effect of the all-E-isomers of these retinoids correlates well with their capacity to bind to RARs and activate RAR/RXR-mediated transcription.

Animals↗

Complementation of an Escherichia coli adhE mutant by the Entamoeba histolytica EhADH2 gene provides a method for the identification of new antiamebic drugs.

The pathogenic protozoan parasite Entamoeba histolytica, the cause of amebic dysentery and amebic liver abscess, is an obligate anaerobe, and derives energy from the fermentation of glucose to ethanol with pyruvate and acetyl coenzyme A as intermediates. We have isolated EhADH2, a key enzyme in this pathway, that is a NAD+- and Fe2+-dependent bifunctional enzyme with acetaldehyde dehydrogenase and alcohol dehydrogenase activities. EhADH2 is the only known eukaryotic member of a newly defined family of prokaryotic multifunctional enzymes, which includes the Escherichia coli AdhE enzyme, an enzyme required for anaerobic growth of E. coli. Because of the critical role of EhADH2 in the amebic fermentation pathway and the lack of known eukaryotic homologues of the EhADH2 enzyme, EhADH2 represents a potential target for antiamebic chemotherapy. However, screening of compounds for antiamebic activity is hampered by the cost of large scale growth of Ent. histolytica, and difficulties in quantitating drug efficacy in vitro. To approach this problem, we expressed the EhADH2 gene in a mutant strain of E. coli carrying a deletion of the adhE gene. Expression of EhADH2 restored the ability of the mutant E. coli strain to grow under anaerobic conditions. By screening compounds for the ability to inhibit the anaerobic growth of the E. coli/EhADH2 strain, we have developed a rapid assay for identifying compounds with anti-EhADH2 activity. Using bacteria to bypass the need for parasite culture in the initial screening process for anti-parasitic agents could greatly simplify and reduce the cost of identifying new therapeutic agents effective against parasitic diseases.

Alcohol Dehydrogenase↗

Molecular cloning and characterization of a transmembrane surface antigen in human cells.

The mouse mAb 6C6, raised against a plasma-membrane preparation from human breast-cancer cells, reacts with an antigen that appears to be overexpressed in human breast cancers and other human tumors. Here we describe the cDNA cloning and characterization of the antigen recognized by the 6C6 mAb. The isolated cDNA clone encodes a protein of 246 amino acids, with a predicted molecular mass of 27 991 Da. The protein contains three amino-terminal hydrophobic regions, which could represent transmembrane domains, and a hydrophilic carboxy-terminal region, which we show to be extracellular. The identity of the protein encoded by the cloned cDNA as the 6C6 antigen was confirmed by in vitro translation and immunoprecipitation experiments, and by transfection into cell lines that do not react with the 6C6 mAb, which resulted in the expression of a 28-kDa surface protein that was recognized by the antibody. The 6C6 antigen appears to be a type II transmembrane protein, with multiple membrane-spanning domains and a long extracellular non-glycosylated carboxy-terminal domain, to which the 6C6 epitope has been mapped. The overall structure of the protein and weak amino acid similarities with a family of multiple-transmembrane-spanning-domain proteins that includes some antigens (such as L6, CD63/ME491 and CO-029) that are overexpressed in tumor cells, suggest that the 6C6 antigen may belong to this family of proteins.

Amino Acid Sequence↗

Germ-line passage is required for establishment of methylation and expression patterns of imprinted but not of nonimprinted genes.

Embryonic stem (ES) cells homozygous for a disruption of the DNA (cytosine-5)-methyltransferase gene (Dnmt) proliferate normally with their DNA highly demethylated but die upon differentiation. Expression of the wild-type Dnmt cDNA in mutant male ES cells caused an increase in methylation of bulk DNA and of the Xist and Igf2 genes to normal levels, but did not restore the methylation of the imprinted genes H19 and Igf2r. These cells differentiated normally in vitro and contributed substantially to adult chimeras. While the Xist gene was not expressed in the remethylated male ES cells, no restoration of the normal expression profile was seen for H19, Igf2r, or Igf2. This indicates that ES cells can faithfully reestablish normal methylation and expression patterns of nonimprinted genes but lack the ability to restore those of imprinted genes. Full restoration of monoallelic methylation and expression was imposed on H19, Igf2, and Igf2r upon germ-line transmission. These results are consistent with the presence of distinct de novo DNA methyltransferase activities during oogenesis and spermatogenesis, which specifically recognize imprinted genes but are absent in the postimplantation embryo and in ES cells.

Alleles↗

T cell responses in calcineurin A alpha-deficient mice.

We have created embryonic stem (ES) cells and mice lacking the predominant isoform (alpha) of the calcineurin A subunit (CNA alpha) to study the role of this serine/threonine phosphatase in the immune system. T and B cell maturation appeared to be normal in CNA alpha -/- mice. CNA alpha -/- T cells responded normally to mitogenic stimulation (i.e., PMA plus ionomycin, concanavalin A, and anti-CD3 epsilon antibody). However, CNA alpha -/- mice generated defective antigen-specific T cell responses in vivo. Mice produced from CNA alpha -/- ES cells injected into RAG-2-deficient blastocysts had a similar defective T cell response, indicating that CNA alpha is required for T cell function per se, rather than for an activity of other cell types involved in the immune response. CNA alpha -/- T cells remained sensitive to both cyclosporin A and FK506, suggesting that CNA beta or another CNA-like molecule can mediate the action of these immunosuppressive drugs. CNA alpha -/- mice provide an animal model for dissecting the physiologic functions of calcineurin as well as the effects of FK506 and CsA.

Animals↗

DNA methyltransferase in normal and Dnmtn/Dnmtn mouse embryos.

The mouse genome experiences a large decrease in net 5-methylcytosine between fertilization and implantation; de novo methylation brings 5-methylcytosine to adult somatic cell levels between implantation and gastrulation. Very little is known of the regulation of demethylation or de novo methylation. Levels of the one known form of DNA methyltransferase are very high in early embryos, but the enzyme is localized to the cytoplasm during most of preimplantation development. We show here that DNA methyltransferase is found exclusively in nuclei of the conceptus after implantation, and that nuclei of proximal decidual cells are free of detectable DNA methyltransferase. High levels of DNA methyltransferase were seen in all tissues, including the developing nervous system, of 9.5- to 12.5-day embryos. The large maternal stores of DNA methyltransferase become limiting prior to embryonic day 9.5, as shown by barely detectable immunostaining in 9.5-day embryos homozygous for a loss-of-function mutation (Dnmtn) in the DNA methyltransferase gene. These mutant embryos failed to develop past the 25-somite stage and showed evidence of developmental delay and some developmental asynchrony. Normal embryonic and extraembryonic tissues contained similar levels of DNA methyltransferase, even though severely reduced methylation levels and a loss of imprinting have previously been observed in extraembryonic tissues. These findings suggest that methylation patterns are not a simple function of the concentration of DNA methyltransferase, and that unidentified factors must be involved in the regulation of de novo methylation during early development of the mouse.

5-Methylcytosine↗

Expression of CD44 splice variants in metastatic and non-metastatic mouse tumour cell lines.

Different splice variants of the CD44 cell-surface molecule have been linked to metastasis formation in several animal and human cancers. We have used metastatic CSML-100 and non-metastatic CSML-0 mouse adenocarcinoma cell lines to determine whether variant CD44 molecules could be implicated in the different behaviour of these cells. Two CD44 splice variants containing exons v7-v10 and v8-v10 were detected in the non-metastatic CSML-0. Two other mouse cell lines, the normal mammary gland NMuMG and the mammary pre-neoplastic CL-S1 were also found to express these exons. A short (hematopoietic) CD44 isoform was expressed in the metastatic CSML-100 and three other mouse mammary tumour cell lines. Overexpression of v7-v10 and v8-v10 CD44 variants in CSML 100 cells did not decrease their metastatic potential.

Alternative Splicing↗

Protozoa. Amebiasis.

The intestinal protozoan parasite Entamoeba histolytica causes amebic dysentery and amebic liver abscess, and ranks third worldwide among parasitic causes of death. The application of molecular techniques to the study of this organism have led to major advances in understanding the pathophysiology of amebic infection. This article reviews what is currently known about the pathogenesis, clinical manifestations, diagnosis, and treatment of amebiasis.

Animals↗