[Treatment of post-operational restenosis of percutaneous transluminal coronary angioplasty with traditional Chinese medicine].
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Angioplasty, Balloon, Coronary↗
Biomedical subjects
J Su
Publications and source records attributed to J Su.
[Clinical study on therapeutic mechanism of Sini Decoction in treating post-percutaneous transluminal coronary angioplasty ischemia-reperfusion injury in terms of syndrome typing of TCM].
OBJECTIVE: To study the mechanism of Sini Decoction (SND) in prevention and treatment of post-percutaneous transluminal coronary angioplasty (PTCA) ischemia-reperfusion injury with different Syndrome typing of TCM. METHODS: Forty patients received PTCA were randomly divided equally into the SND group and the control group, in each group, there were 10 of Excess Syndrome (ES) and 10 of Deficiency Syndrome (DS). Twenty-five ml of SND was given daily to the SND group from 3 days before operation to the third day after operation. The blood superoxide dismutase (SOD) activity, malondialdehyde (MDA) and nitric oxide (NO) content of patients were determined before PTCA, and 1 hrs, 12 hrs, 24 hrs, 48 hrs and 72 hrs after PTCA. RESULTS: Before PTCA, the cases of DS were characterized by low SOD activity and high MDA content, as compared with the patients of ES, P < 0.05. SND could relieve the post-PTCA deprivation of SOD activity and NO content and the elevation of MDA level of both ES and DS patients, the amplitude of elevation of SOD activity in DS patients was higher than that in ES patients (P < 0.05). CONCLUSION: SND has antagonisting effect on post-PTCA ischemia-reperfusion injury, which is more effective in treating patients with DS.
Angioplasty, Balloon, Coronary↗
[Study on the steroid constituents of soft coral Lobophytum microspiculatum].
The soft coral Lobophytum microspiculatum collected from Xisa Islands of the South China Sea was immersed in and extracted with ethyl alcohol and the extract was concentrated, and then partitioned between ethyl acetate and water. The portion soluble in ethyl acetate was subjected to column chromatography over Sillca H, eluted with a step gradient of EtOAc and petroleum ether. The sterols were obtained from 20% EtOAc-petroleum ether eluent portion. By means of GC/MS method, the sterols were identified to be: cholesta-26-methyl-ol; ergosta-8, 22-dien-3 beta-ol, 24-methyl; ergosta-5, 22-dien-3 beta-ol, 23, 24-dimethyl; cholesta-5,22(23)-dien-3 beta-ol, 22,24-dimethyl; cholesterol; ergosta-5,22-dien-3 beta-ol, 24-methyl; ergosta-5,22-dien-3 beta-ol, 22,24-dimethyl, 24-methyl-cholesterol; ergosta-7-en-3 beta-ol, 24-methyl; nor-ergosta-7-en-3 beta-ol and gorgosterol. Among them cholest-5,22(23)-3 beta-ol, 22,24-dimethyl (4) is a new compound which was found at the first time from the nature. This finding gave a further prove for the biogenesis path way of gorgosterol.
Animals↗
Enhancement of aflatoxin B1-induced enzyme altered hepatic foci in rats by treatment with carbon tetrachloride.
The effect of carbon tetrachloride (CCl4) on aflatoxin B1 (AFB1)-induced enzyme altered hepatic foci has been examined in young male Fischer rats given AIN-76A diet. A single i.p. dose of AFB1 (0.2 mg/kg body wt) was given to rats 24 h after partial hepatectomy. Two weeks later, CCl4 (0.8 ml/kg body wt) was injected i.p. once a week for 9 weeks. Animals were sacrificed 24 h after the last dose of CCl4 and glutathione S-transferase placental form (GST-P) and gamma-glutamyl transpeptidase (GGT) positive hepatic foci were analyzed by immunohistochemical and histochemical methods, respectively. Ten weeks after AFB1 dosing, treatment with CCl4 increased the number of AFB1-induced enzyme altered foci several fold and produced a ten to twenty-fold increase in area and volume. GST-P was more sensitive than GGT in detecting AFB1-induced enzyme altered foci. Treatment with AFB1 or CCl4 produced mild hepatic fibrosis in zones 1 and 3 respectively, whereas both treatments produced severe fibrosis in zones 1 to 3 areas. Treatment with CCl4 after AFB1 dosing lowered hepatic GSH levels by 20% and increased lipid peroxidation by 40%. It appears that CCl4, by being an effective enhancer of AFB1-induced enzyme altered hepatic foci in the rat, may mimic cirrhosis observed in human hepatocellular carcinoma.
Aflatoxin B1↗
Cystatin F is a glycosylated human low molecular weight cysteine proteinase inhibitor.
A previously undescribed human member of the cystatin superfamily called cystatin F has been identified by expressed sequence tag sequencing in human cDNA libraries. A full-length cDNA clone was obtained from a library made from mRNA of CD34-depleted cord blood cells. The sequence of the cDNA contained an open reading frame encoding a putative 19-residue signal peptide and a mature protein of 126 amino acids with two disulfide bridges and enzyme-binding motifs homologous to those of Family 2 cystatins. Unlike other human cystatins, cystatin F has 2 additional Cys residues, indicating the presence of an extra disulfide bridge stabilizing the N-terminal region of the molecule. Recombinant cystatin F was produced in a baculovirus expression system and characterized. The mature recombinant protein processed by insect cells had an N-terminal segment 7 residues longer than that of cystatin C and displayed reversible inhibition of papain and cathepsin L (Ki = 1.1 and 0.31 nM, respectively), but not cathepsin B. Like cystatin E/M, cystatin F is a glycoprotein, carrying two N-linked carbohydrate chains at positions 36 and 88. An immunoassay for quantification of cystatin F showed that blood contains low levels of the inhibitor (0.9 ng/ml). Six B cell lines in culture secreted barely detectable amounts of cystatin F, but several T cell lines and especially one myeloid cell line secreted significant amounts of the inhibitor. Northern blot analysis revealed that the cystatin F gene is primarily expressed in peripheral blood cells and spleen. Tissue expression clearly different from that of the ubiquitous inhibitor, cystatin C, was also indicated by a high incidence of cystatin F clones in cDNA libraries from dendritic and T cells, but no clones identified by expressed sequence tag sequencing in several B cell libraries and in >600 libraries from other human tissues and cells.
Amino Acid Sequence↗
Localisation of the nitric oxide (NO)/cGMP-pathway in the vestibular system of guinea pigs.
The exact distribution of nitric oxide-synthases (NOS) in the vestibular system has not been described satisfying yet. Immunostaining, using specific antibodies to the three known NOS-isoforms, to cyclic guanosine monophosphate (cGMP) and soluble guanylyl-cyclase (sGC), the second messenger system of nitric oxide (NO), was performed on paraffin sections of temporal bone from guinea pigs. eNOS could be detected in vestibular ganglion cells and in nerve fibres, including the calyces, surrounding the type 1 hair cells (HC). bNOS was found in the sensory epithelium, ganglion cells and in bone, while iNOS could not be found. NOS-detection was accompanied by reactivity to sGC and to cGMP. This finding implies that b- and eNOS-generated NO is involved in regulative processes in neurotransmission and regulation of blood flow.
Animals↗
cDNA cloning, tissue distribution, and substrate characteristics of a cis-Retinol/3alpha-hydroxysterol short-chain dehydrogenase isozyme.
We report here a mouse cDNA that encodes a 316-amino acid short-chain dehydrogenase that prefers NAD+ as its cofactor and recognizes as substrates androgens and retinols, i.e. has steroid 3alpha- and 17beta-dehydrogenase and cis/trans-retinol catalytic activities. This cis-retinol/androgen dehydrogenase type 2 (CRAD2) shares close amino acid similarity with mouse retinol dehydrogenase isozyme types 1 and 2 and CRAD1 (86, 84, and 87%, respectively). CRAD2 exhibits cooperative kinetics with 3alpha-adiol (3alpha-hydroxysteroid dehydrogenase activity) and testosterone (17beta-hydroxysteroid dehydrogenase activity), but Michaelis-Menten kinetics with androsterone (3alpha-hydroxysteroid dehydrogenase activity), 11-cis-retinol, all-trans-retinol, and 9-cis-retinol, with V/K0.5 values of 1.6, 0.2, 0.1, 0.04, 0.005, and not saturated, respectively. Carbenoxolone (IC50 = 2 microM) and 4-methylpyrazole (IC50 = 5 mM) inhibited CRAD2, but neither ethanol nor phosphatidylcholine had marked effects on its activity. Liver expressed CRAD2 mRNA intensely, with expression in lung, eye, kidney, and brain (2.9, 2, 1.6, and 0.6% of liver mRNA, respectively). CRAD2 represents the fifth isozyme in a group of short-chain dehydrogenase/reductase isozymes (retinol dehydrogenases 1-3 and CRAD1), closely related in primary amino acid sequence (approximately 85%), that are expressed in different quantities in various tissues, have different substrate specificities, and may serve different physiological functions. CRAD2 may alter the amounts of active and inactive androgens and/or convert retinols into retinals. These data expand insight into the multifunctional nature of short-chain dehydrogenases/reductases and into the enzymology of steroid and retinoid metabolism.
Alcohol Oxidoreductases↗
TRANK, a novel cytokine that activates NF-kappa B and c-Jun N-terminal kinase.
We searched the expressed sequence tag database using sequence homology and identified a novel cytokine, which we have named TRANK (thioredoxin peroxidase-related activator of NF-kappa B and c-Jun N-terminal kinase). The predicted amino acid sequence of TRANK was highly homologous to that of the thiol-specific antioxidant proteins. Unlike these proteins, however, TRANK had a putative secretory signal polypeptide and was found to be secreted by cells. TRANK was expressed in most tissues and cell lines, and the gene that encodes it was mapped to chromosome Xp21-22.1. TRANK activated NF-kappa B and induced the degradation of the inhibitory subunit of NF-kappa B. In addition, TRANK up-regulated the expression of NF-kappa B-dependent gene products, ICAM-1, and inducible nitric oxide synthase. TRANK also activated c-Jun N-terminal kinase and induced the proliferation of normal human foreskin fibroblasts. Its homology with antioxidant proteins, wide distribution in tissues, and ability to activate NF-kappa B and c-Jun N-terminal kinase suggest that TRANK plays an important role in inflammation.
Amino Acid Sequence↗
Expression, purification, and bioassay of human stanniocalcin from baculovirus-infected insect cells and recombinant CHO cells.
Stanniocalcin is a calcium- and phosphate-regulating glycoprotein hormone that was first described in fish where it functions in preventing hypercalcemia. Human cDNA clones encoding the homolog of stanniocalcin have been recently isolated. In this study, the full-length cDNA coding for human stanniocalcin (hSTC) was cloned into both baculovirus and CHO expression vectors. Recombinant hSTC was then produced efficiently from both baculovirus-infected insect cells and CHO cells in large-scale bioreactors. Purification protocols were developed and used to purify recombinant hSTC from both sources in four chromatography steps. The hSTCs from both expression systems were secreted as glycosylated proteins and as disulfide-linked homodimers. The results from glycosylation studies indicated that stanniocalcin from both sources contained N-linked oligosaccharides but no O-linked sugars. In an in vivo bioassay based on the inhibition of gill calcium transport in fishes, the baculovirus and CHO-expressed protein showed biological activity which is dose dependent. The inhibitory effects of hSTC produced from both systems were essentially equipotent in fishes, despite the differences in glycosylation. Consequently, the precise role of the carbohydrate moiety in recombinant hSTC remains to be determined.
Amino Acid Sequence↗
Unanticipated admission after ambulatory surgery--a prospective study.
PURPOSE: To determine the incidence, the reasons, and the predictive factors for unanticipated admission after ambulatory surgery. METHODS: Preoperative, intraoperative, and postoperative data were collected prospectively on 15,172 consecutive ambulatory surgical patients during a 32-month period. The data were built into a statistical model, and predictive factors were identified and classified. RESULTS: The overall incidence of unanticipated admission was 1.42%. Admitted patients were more likely to be older, male, and ASA status II or III. Duration of anaesthesia was longer, and surgery was more likely to be completed after 3 pm. Length of stay in the Postanaesthesia Care Unit and the Ambulatory Surgery Unit was longer. Surgical reasons were cited in 38.1% of admitted patients; anaesthesia-related reasons were cited in 25%; social reasons accounted for 19.5%, and medical reasons for 17.2%. Ear, nose and throat (ENT) patients had the highest unanticipated admission rate (18.2%), followed by urology (4.8%) and chronic pain block (3.9%). Gynaecological patients had the lowest rate (0.4%). Among the predictive factors found were male, ASA status II and III, long duration of surgery, surgery finishing after 3 pm, postoperative bleeding, excessive pain, nausea and vomiting, and excessive drowsiness or dizziness. CONCLUSION: Earlier operating time for certain surgical procedures, screening for proper support at home, and implementation of clinical pathways to deal aggressively with problems such as pain, nausea and vomiting should decrease the incidence of unanticipated admission.
Ambulatory Surgical Procedures↗
High expression of stanniocalcin in differentiated brain neurons.
Stanniocalcin (STC) is a glycoprotein hormone first found in fish, in which it regulates calcium homeostasis and protects against hypercalcemia. Human and mouse stc cDNA were recently cloned. We found a dramatically upregulated expression of STC during induced neural differentiation in a human neural crest-derived cell line, Paju. Immunohistochemical staining of sections from human and adult mouse brain revealed abundant presence of STC in the neurons with no activity in the glial cells. STC expression was not seen in immature brain neurons of fetal or newborn mice. Given that STC has been found to regulate calcium/phosphate metabolism in some mammalian epithelia, we suggest that STC may act as a regulator of calcium homeostasis in terminally differentiated brain neurons.
Animals↗
Acute effects of an endothelin-1 receptor antagonist bosentan at different stages of heart failure in conscious dogs.
OBJECTIVE: Inhibition by endothelin antagonist is a potential therapy in heart failure. However, the effect of endothelin inhibition during the development of heart failure has not been evaluated. The goal of our study was to examine the acute hemodynamic effects of the mixed endothelin receptor antagonist bosentan in the control state and at different stages of heart failure induced by right ventricular pacing (250 bpm) in conscious dogs. METHODS: Nine dogs were chronically instrumented for the measurements of left ventricular pressure and its first derivative (dP/dt), cardiac output, left ventricular regional wall thickness and aortic pressure. Bosentan (3 mg/kg, i.v. bolus) and placebo were given at control, at 1 week of pacing (stage of left ventricular dysfunction with perserved cardiac output) and at 3 weeks of pacing (phase of heart failure with low cardiac output). RESULTS: With the development of heart failure, baseline plasma endothelin level increased progressively. Placebo did not induce hemodynamic and plasma endothelin changes during the 30 min recording at any stage. At control, bosentan did not change hemodynamics. At 1 and 3 weeks of pacing, bosentan did not modify left ventricular myocardial function indices but reduced mean arterial pressure (by 7 +/- 2 and 8 +/- 1 mm Hg respectively, p < 0.005). Bosentan increased stroke volume at 3 weeks of pacing only. CONCLUSIONS: Endothelin inhibition by endothelin antagonist bosentan, decreases aortic pressure in both early left ventricular dysfunction and in heart failure in contrast with the control state. In the phase of heart failure with low cardiac output, bosentan increases stroke volume. In the early left ventricular dysfunction, bosentan, by reducing arterial pressure, may limit the deterioration of cardiac function through a reduction of the workload imposed on the heart.
Animals↗
Lung transplantation in Sauropus androgynus consumption patients in Taiwan.
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Adult↗
Small intestine bacterial overgrowth presenting as protein-losing enteropathy.
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Adult↗
Identification of multiple forms of 180-kDa ribosome receptor in human cells.
Herein, we describe the analysis and mapping of cDNA clones encoding variant forms of the human homolog of the canine 180-kDa ribosome receptor (p180). One form, similar to the chicken ES/130 homolog, possesses a large uninterrupted C-terminal region composed predominantly of heptad repeats predicted to form an alpha-helical double-stranded coiled-coil rod. Other forms contain in addition a 10-amino acid consensus motif, NQGKKAEGAQ, repeated up to 54 times in tandem close to the N-terminus. Such repeats in canine p180 represent a ribosome-binding domain. The cDNA hybridized to a major 6-kb transcript in all tissues examined, where very high expression was observed in tissues that carry out a high level of secretion such as pancreas, liver, and placenta. The ES130/p180 gene was mapped to chromosome 20p12, and a potential pseudogene appears to reside on chromosome 7. In summary, the data suggest that p180 exists in humans in different forms because of complete removal of tandem repeats, or partial intraexonic splicing, creating different repeat lengths with potentially novel ribosome-binding characteristics.
Alternative Splicing↗
TR1, a new member of the tumor necrosis factor receptor superfamily, induces fibroblast proliferation and inhibits osteoclastogenesis and bone resorption.
A newly identified member of the tumor necrosis factor receptor (TNFR) superfamily shows activities associated with osteoclastogenesis inhibition and fibroblast proliferation. This new member, called TR1, was identified from a search of an expressed sequence tag database, and encodes 401 amino acids with a 21-residue signal sequence. Unlike other members of TNFR, TR1 does not contain a transmembrane domain and is secreted as a 62 kDa glycoprotein. TR1 gene maps to chromosome 8q23-24.1 and its mRNA is abundantly expressed on primary osteoblasts, osteogenic sarcoma cell lines, and primary fibroblasts. The receptors for TR1 were detected on a monocytic cell line (THP-1) and in human fibroblasts. Scatchard analyses indicated two classes of high and medium-high affinity receptors with a kD of approximately 45 and 320 pM, respectively. Recombinant TR1 induced proliferation of human foreskin fibroblasts and potentiated TNF-induced proliferation in these cells. In a coculture system of osteoblasts and bone marrow cells, recombinant TR1 completely inhibited the differentiation of osteoclast-like multinucleated cell formation in the presence of several bone-resorbing factors. TR1 also strongly inhibited bone-resorbing function on dentine slices by mature osteoclasts and decreased 45Ca release in fetal long-bone organ cultures. Anti-TR1 monoclonal antibody promoted the formation of osteoclasts in mouse marrow culture assays. These results indicate that TR1 has broad biological activities in fibroblast growth and in osteoclast differentiation and its functions.
Animals↗
Dehydration-stress-regulated transgene expression in stably transformed rice plants
To confer abscisic acid (ABA) and/or stress-inducible gene expression, an ABA-response complex (ABRC1) from the barley (Hordeum vulgare L.) HVA22 gene was fused to four different lengths of the 5' region from the rice (Oryza sativa L.) Act1 gene. Transient assay of beta-glucuronidase (GUS) activity in barley aleurone cells shows that, coupled with ABRC1, the shortest minimal promoter (Act1-100P) gives both the greatest induction and the highest level of absolute activity following ABA treatment. Two plasmids with one or four copies of ABRC1 combined with the same Act1-100P and HVA22(I) of barley HVA22 were constructed and used for stable expression of uidA in transgenic rice plants. Three Southern blot-positive lines with the correct hybridization pattern for each construct were obtained. Northern analysis indicated that uidA expression is induced by ABA, water-deficit, and NaCl treatments. GUS activity assays in the transgenic plants confirmed that the induction of GUS activity varies from 3- to 8-fold with different treatments or in different rice tissues, and that transgenic rice plants harboring four copies of ABRC1 show 50% to 200% higher absolute GUS activity both before and after treatments than those with one copy of ABRC1.
Journal Article↗
Early captopril treatment prevents hypertrophydependent gene expression in hearts of SHR.
Treatment of spontaneously hypertensive rats (SHR) with captopril (100 mg . kg-1 . day-1) throughout development and during the first 16 wk of life leads to a reduction in blood pressure and left ventricular hypertrophy. Blood pressures and hypertrophy are reduced in these animals (vs. untreated SHR) for up to 24 wk after discontinuation of the drug. We used conventional blot hybridization and Western analysis to examine hypertrophy-dependent gene expression during this period. Ventricular expression of the atrial natriuretic peptide gene was reduced by >90% at 16 wk of age in the captopril-treated SHR. Expression increased in the 24 wk after discontinuation of treatment, but remained well below that of the untreated SHR. A similar reduction in ventricular c-myc gene expression was seen with captopril treatment. Neither renal expression of the atrial natriuretic peptide gene nor ventricular expression of the c-fos gene was affected by captopril. This study demonstrates that captopril treatment during a critical period of development in the SHR leads to a sustained reduction in hypertrophy-dependent myocardial gene expression, which does not revert to levels seen in the untreated SHR after discontinuation of the drug.
Animals↗