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Biomedical subjects

L Yu

Publications and source records attributed to L Yu.

At least 667 records · Page 37Linked to original sources
PubMed1993

Extended survival and function of peripheral nerve allografts after cessation of long-term cyclosporin administration in rats.

To determine whether survival and function of peripheral nerve allografts are possible after cessation of long-term cyclosporin (CsA) treatment, we grafted 4.25 cm Lewis rat peripheral nerve allografts (n = 22) into tibial nerve gaps in recipient brown Norway rats. Allograft groups received CsA (15 mg/kg) subcutaneously every day for 20 days and then biweekly for either 5 or 8 months after transplantation. The control group, brown Norway rats with isografts from brown Norway donor rats (n = 2), also received identical CsA treatment. Semimonthly electrophysiologic studies were done from postoperative week 13 until the animals were killed (up to 79 weeks). The corresponding CsA levels in the nerve and blood were recorded from cessation of CsA up to 58 weeks after surgery. No electrophysiologic signs of rejection were observed in any of the 22 allograft recipients treated with CsA for up to 8 months or in 17 of the 22 observed for up to 58 weeks after cessation of CsA. Overall, 5 of 22 allografts were rejected in the first 8 weeks after discontinuation of CsA. Signs of rejection occurred only in the 5-month treatment group and followed the large initial drop in CsA blood level (from 1010 ng/ml to < 25 ng/ml) that occurred within the first 6 weeks after CsA cessation. The two isograft controls demonstrated no electrophysiologic signs of rejection up to 58 weeks after surgery. Peripheral nerve allografts in the rat can regenerate and function on long-term CsA; after cessation of CsA, they can function for extended periods of time without signs of rejection if trace amounts of CsA are present.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1993

Calcium potentiates cyclic AMP stimulation of pineal arylalkylamine N-acetyltransferase.

Pineal arylalkylamine N-acetyltransferase (N-acetyltransferase) controls large daily changes in melatonin production. It is generally thought that the activity of this enzyme is controlled by norepinephrine acting exclusively via elevation of cyclic AMP. However, norepinephrine also elevates pineal intracellular Ca2+ concentration ([Ca2+]i), and it is not known whether Ca2+ is involved in regulating N-acetyltransferase activity other than through its established role in cyclic AMP production. In this study, the issue of whether Ca2+ enhances the effects of cyclic AMP on N-acetyltransferase activity was investigated. The effects of cyclic AMP protagonists (isobutylmethylxanthine, N6,2'-O-dibutyryladenosine 3',5'-cyclic monophosphate, 8-bromoadenosine 3',5'-cyclic monophosphate, and adenosine 3',5'-cyclic monophosphothioate, Sp-diastereomer) were examined in combination with [Ca2+]i protagonists (A23187, ionomycin, and phenylephrine). All [Ca2+]i protagonists potentiated the effects of cyclic AMP protagonists. For example, ionomycin potentiated the effects of low concentrations of 8-bromoadenosine 3',5'-cyclic monophosphate, and A23187 potentiated the effects of isobutylmethylxanthine without altering cyclic AMP accumulation. These findings indicate that Ca2+ and cyclic AMP probably act physiologically in a coordinated manner to stimulate N-acetyltransferase activity; these second messengers could act directly at one or more sites or through indirect actions mediated by kinases.

1-Methyl-3-isobutylxanthine↗
PubMed1993

[Allergic granulomatous angiitis].

Allergic granulomatous angiitis (AGA) is a rare disease, which varies in clinical manifestation. The clinical course includes three stages. In the first stage most of the patients show symptoms of respiratory disease, 82 per cent of the patients has asthma and 88 per cent chronic rhinitis. In the second stage there is blood eosinophilia and in the last stage involvement of multiple organs. The etiology is not yet clear. Since 1982 four cases of AGA have been encountered in PUMC Hospital, but they were all diagnosed after 1988. All were male and aged 36-54 years. Two of them had asthma history and three enlargement of liver and proteinuria, ECG showed heart block in two, all four had neuromuscular and cutaneous involvement and elevated blood eosinophil with absolute number ranging from 1254 to 8104/mm3. Biopsy from different sites showed panangiitis associated with eosinophil infiltration and/or granulomatosis formation. All were sensitive to prednisone therapy with or without CTX after treatment the absolute eosinophil count in the four patients was less than 1000/mm3 and the symptoms alleviated.

Adult↗
PubMed1993

Calcium modulation and cell injury in isolated rat proximal tubules.

The possible role of an increased calcium influx in mediating hypoxia-induced injury in isolated rat proximal tubules was examined. Reduction of extracellular calcium delayed the development of proximal tubule cell injury as reflected by the release of lactate dehydrogenase (LDH). This protection, as assessed by LDH release, was not associated with improvements of cell ATP or potassium concentrations. The calcium channel blocker verapamil also delayed the development of cell injury due to hypoxia. This protective effect was evident in the presence of normal or low extracellular calcium. Specifically, hypoxic tubules incubated in low calcium medium were further protected by the addition of verapamil. The protection with verapamil was evident not only by diminished LDH release, but also by improvements in cell ATP and potassium concentration. Further experiments demonstrated that verapamil also increased cell potassium levels in control oxygenated tubules incubated in normal calcium medium. Thus, the results demonstrate that low calcium medium delays the onset of cell membrane injury during hypoxia as assessed by LDH release. The protective effects of verapamil can be demonstrated in the presence of normal or low calcium media, and involve not only diminished LDH release but also increased cell ATP and potassium concentrations. Therefore, in addition to any effect on calcium influx, the effect of verapamil appears to involve a protective effect at cell membrane or mitochondria sites.

Adenosine Triphosphate↗
PubMed1993

An epidemiological study of hemoglobin levels and prevalence of anemia in young children from Bas-Zaire.

A population of 183 Zairean infants and young children (0.5 to 48 months old) who lived in rural Bas-Zaire has been examined in regard to hemoglobin (Hb), hematocrit (Hct) and mean corpuscular hemoglobin concentration (MCHC). The mean Hb was 9.03 g/dL, Hct 28.4%, and MCHC 30.7 micrograms/dL. These means are below normal by WHO and/or American Academy of Pediatrics criteria. Although there was no significant sex difference in the mean hematoglobin measurements, boys more than 24 months old had a higher mean Hb (9.98 g/dL) than girls (8.59d g/L) of the same age. Approximately 80%, 76% and 56% of children had Hb < 11 g/dL, Hct < 34% and MCHC < 32 micrograms/dL respectively. The highest prevalence of anemia was between the age of 12 and 18 months. Severe anemia (Hb < 8 g/dL) was observed in 30.65% of the study population (26.6% boys and 34.8% girls). Approximately one third of children had very low Hct levels (< or = 25%). Based on MCHC, iron deficiency was likely responsible of the anemia in 61% of the children. Both Hb (p < 0.05) and Hct positively correlated with the mother's level of education. Because of the many detrimental effects of iron deficiency in infants and young children on immunity, psychomotor, behaviour and mental development routine assessment of iron status and correction of iron deficiency should become a part of the Surveillance Programme in this population.

Anemia, Hypochromic↗
PubMed1993

Molecular cloning and functional expression of a mu-opioid receptor from rat brain.

Opioid drugs act on specific receptors to modulate a wide range of physiological functions. There are at least three types of opioid receptors, mu, delta, and kappa. Using a cDNA probe for a mouse delta-opioid receptor in low stringency hybridization, a clone has been isolated from a rat brain cDNA library. This clone contains an open reading frame of 1194 base pairs, with a deduced polypeptide of 398 amino acid residues. The predicted protein exhibits the structural features of guanine nucleotide-binding protein-coupled receptors and displays a high degree of sequence homology with the mouse delta-opioid receptor. When transfected into COS-7 cells, the cDNA conferred a binding site with subnanomolar affinity for [3H]diprenorphine, a high affinity ligand for all three types of opioid receptors. This site also displayed nanomolar affinity for [D-Ala2,N-Me-Phe4,Gly-ol5]-enkephalin (DAGO), a mu-selective agonist, whereas its affinities for the delta-selective agonist [D-Pen2,5]-enkephalin and the kappa-selective agonist U-50488 were in the micromolar range. Several mu-selective antagonists, including naloxonazine, beta-funaltrexamine, and cyprodime, were capable of displacing [3H]diprenorphine binding with nanomolar potency. The pharmacological profile of this binding site thus suggests that it is a mu-type opioid receptor, which we designated MOR-1. In COS-7 cells expressing MOR-1 and stimulated with forskolin, treatment with DAGO decreased the steady state levels of cAMP; this inhibitory effect of DAGO was blocked by naloxonazine. These results suggest that this mu-opioid receptor is functionally coupled to the inhibition of adenylyl cyclase.

Amino Acid Sequence↗
PubMed1993

Infusion of glycine does not attenuate in vivo ischemic acute renal failure in the rat.

Recent in vitro studies have demonstrated that the amino acid glycine affords profound protection against hypoxic injury in isolated rat proximal tubules and the isolated perfused rat kidney. In the present study we have examined the in vivo effect of glycine in a rat model of ischemic acute renal failure. Acute renal failure was induced in rats by right uninephrectomy and clamping of the left renal artery for 45 or 60 minutes. Glycine infusion was initiated 60 minutes before renal artery clamping at a rate to increase serum glycine levels above 2.0 mmol/L. Control rats received a 5% dextrose infusion. In the control rats, both 45 minutes and 60 minutes of clamping resulted in reversible acute renal failure and a serum creatinine level after 24 hours averaging 2.1 +/- 0.3 mg/dl (mean +/- SEM) and 3.3 +/- 0.4 mg/dl, respectively. Glycine treatment did not attenuate the decrease of renal function in the 45-minute and 60-minute models, with serum creatinine averaging 2.1 +/- 0.4 mg/dl and 3.4 +/- 0.5 mg/dl, respectively. Histologic examination also did not reveal any differences between control and glycine-treated rats. Therefore, we conclude that infusion of glycine does not afford in vivo protection against acute ischemic renal injury in the rat. The in vitro protective effects of glycine therefore cannot be extrapolated to the in vivo situation.

Acute Kidney Injury↗
PubMed1992

Cytochrome b560 (QPs1) of mitochondrial succinate-ubiquinone reductase. Immunochemistry, cloning, and nucleotide sequencing.

Mitochondrial succinate-ubiquinone reductase is composed of two parts, a water-soluble succinate dehydrogenase and a two-polypeptide membrane-anchoring protein fraction (QPs). The larger polypeptide of QPs is believed to be associated with cytochrome b560 (QPs1). The structure of QPs1 was studied by immunochemistry and molecular cloning and sequencing. Antibodies against QPs1 were raised in rabbits, purified, and characterized by enzyme-linked immunosorbent assay and Western blotting. The purified antibodies inhibited 75% of the reconstitutive activity of QPs and reacted with both submitochondrial particles (SMP) and mitoplasts. The binding of these antibodies to SMP was greatly increased when succinate dehydrogenase was removed from SMP by alkaline treatment, indicating that QPs1 is a transmembranous protein and that some of its specific epitopes are covered by succinate dehydrogenase. Anti-QPs1 antibodies were used to screen one cDNA clone encoding QPs1 from a bovine heart cDNA lambda gt11 expression library. The cDNA insert is 946 base pairs with an open reading frame of 396 base pairs that encodes for 132 amino acid residues. The molecular weight of QPs1, calculated from the deduced amino acid sequence, is 14,320. Although the apparent molecular weight of QPs1, estimated by high resolution SDS-polyacrylamide gel electrophoresis, is approximately 11,000, the existence of a presequence was ruled out by mass spectrometric analysis of protein fragments. QPs1 is a very hydrophobic protein. Three probable membrane-spanning segments were revealed by a hydropathy plot of the sequence. QPs1 has a higher sequence similarity to the sdhC peptide of Escherichia coli than to the sdhC peptide (cytochrome b558) of Bacillus subtilis. Like the bacterial proteins, QPs1 has 2 conserved histidines at positions 34 and 90. The conserved nature and similar location of these 2 histidines, on the matrix-side surface of the membrane, suggest that they are involved in heme ligation of cytochrome b560.

Amino Acid Sequence↗
PubMed1992

Determination of the nicotine metabolite trans-3'-hydroxycotinine in urine of smokers using gas chromatography with nitrogen-selective detection or selected ion monitoring.

A gas chromatographic method for the determination of the nicotine metabolite trans-3'-hydroxycotinine is described. The method involves conversion of the metabolite to the tert.-butyldimethylsilyl derivative, chromatography on a fused-silica capillary column, and determination using nitrogen-phosphorus detection or electron ionization mass spectrometry with selected ion monitoring. A structural analogue, trans-3-hydroxy-1-methyl-5-(2-pyridyl)pyrrolidin-2-one (trans-3'-hydroxy-ortho-cotinine), was used as an internal standard. Using selected ion monitoring, good precision and accuracy were obtained for determination of trans-3'-hydroxycotinine in urine over the concentration range 10-10,000 ng/ml. There was a good correlation between concentrations determined by selected ion monitoring and by nitrogen-phosphorus detection in urine of smokers, although low concentrations determined using nitrogen-phosphorus detection tended to be somewhat higher, suggesting some interference from urinary constituents. Concentrations and 24-h excretion of trans-3'-hydroxycotinine in the urine of 22 cigarette smokers are reported and compared to concentrations and excretion of nicotine, cotinine, nicotine 1'-N-oxide, nornicotine, and cotinine N-oxide.

Chromatography, Gas↗
PubMed1992

Spin-label electron paramagnetic resonance and differential scanning calorimetry studies of the interaction between mitochondrial cytochrome c oxidase and adenosine triphosphate synthase complex.

The interaction between cytochrome c oxidase complex and adenosine triphosphate synthase (F1F0) complex in the purified, dispersed state and embedded in phospholipid vesicles was studied by differential scanning calorimetry and by spin-label electron paramagnetic resonance. The detergent-dispersed cytochrome oxidase and F1F0 complexes undergo endothermic thermodenaturation. However, when these complexes are embedded in phospholipid vesicles, they undergo exothermic thermodenaturation. The energy released is believed to result from the collapse of a strained interaction between unsaturated fatty acyl groups of phospholipids and an exposed area of the complex formed by the removal of interacting proteins. The exothermic enthalpy change of thermodenaturation of a protein-phospholipid exothermic enthalpy change of thermodenaturation of a protein-phospholipid vesicle containing both cytochrome oxidase complex and F1F0 was smaller than that of a mixture of protein-phospholipid vesicles formed from each individual electron transfer complex. This suggests specific interaction between cytochrome oxidase complex and F1F0 in the membrane. Further evidence for interaction between these two complexes is provided by saturation transfer EPR studies in which the rotational correlation time of spin-labeled cytochrome oxidase increases significantly when the complex is mixed with F1F0 prior to being embedded in phospholipid vesicles. From these results, it is concluded that at least a part of cytochrome oxidase and a part of F1F0 form a supermacromolecular complex in the inner mitochondrial membrane. No such supermacromolecular complex is detected between F1F0 and ubiquinol--cytochrome c reductase.

Animals↗
PubMed1992

Prevalence of human papillomavirus types 16 and 18 in squamous-cell carcinoma of the penis: a retrospective analysis of primary and metastatic lesions by differential polymerase chain reaction.

Human papillomaviruses (HPV), particularly types 16 and 18, may be carcinogenic effectors in a variety of human lower-genital-tract malignancies. Using the highly sensitive technique of differential polymerase chain reaction (D-PCR) with amplimers from the E6 open reading frames of HPV types 16 and 18, a retrospective analysis of a 20-year institutional experience with squamous-cell carcinoma of the penis (SCCP) was performed to determine the prevalence of these HPV types in this malignancy. Paraffin-embedded surgical specimens of primary (N = 27), locally recurrent (N = 5), and metastatic deposits (N = 26) from 29 patients with invasive SCCP were analyzed, as well as primary (N = 3) and recurrent (N = 2) specimens from 2 patients with penile carcinoma in situ (CIS) (Bowen's disease). Nine of the 29 (31%) patients had invasive SCCP containing HPV 16 or 18 DNA, with HPV 16 found in 8 (28%) and HPV 18 in I (3%); no patient had both. In 7 patients in which only tissue from metastatic sites was available, 2 had HPV 16 detected in 2 separate metastatic sites each. Specimens from both primary and metastatic sites were available in an additional 6 patients, and HPV 16 was detected in specimens from 3 of these 6 patients. HPV was detected in comparable copy number at both sites in each patient, indicating that HPV DNA may be a stable component within cancer cells during disease progression. Of patients with CIS only, 1 of 2 was positive for HPV 16, and upon multifocal recurrence, showed persistence of the virus at 2 separate sites. Southern blotting was performed to confirm the presence of type-specific HPV DNA and showed complete concordance with D-PCR, but discordant hybridization intensities for HPV 18 were noted between the control and positive patient specimens; sequence analysis of the patient specimen revealed 4 point mutations in the HPV-18 target segment. Comparison of the HPV-positive (both HPV 16 and HPV 18) and HPV-negative groups revealed no statistical differences between groups in patients age or ethnic origin, tumor histologic grade, or incidence of nodal involvement. Kaplan-Meier analysis of both overall and cause-specific survival likewise was not different between groups. These data, particularly the presence of HPV in metastatic deposits, provide strong evidence for an etiologic role of HPV type 16 (and possibly 18) in a substantial sub-set of patients from the southeastern United States who developed SCCP.

Aged↗
PubMed1992

Characterization of ubisemiquinone radicals in succinate-ubiquinone reductase.

A thenoyl trifluoroacetone-sensitive and antimycin-insensitive ubisemiquinone radical (Qs) is readily detected in purified succinate-cytochrome c reductase. When this reductase is resolved into succinate-Q and ubiquinol-cytochrome c reductases, Qs was not detected in either reductase. The difficulty in detecting such a radical in purified succinate-Q reductase has puzzled investigators for years. A deficiency of Q in the isolated complex is the reason for the failure to detect Qs. Upon addition of exogenous Q, a thenoyl trifluoroacetone-sensitive Q-radical is readily detectable in isolated succinate-Q reductase under a controlled redox potential. Maximum radical concentration is observed when 5 mol of exogenous Q, per mole of flavin, is added. The radical gives an EPR signal with a g-value of 2.005 and a line-width of 12 G. The Em of Qs is 84 mV at pH 7.4, with half-potentials of E1 = 40 mV and E2 = 128 mV. The Qs-radical does not show power saturation, even at 200 mW.

Antimycin A↗
PubMed1992

Further studies of the ability of xyloglucan oligosaccharides to inhibit auxin-stimulated growth.

The structural features required for xyloglucan oligosaccharides to inhibit 2,4-dichlorophenoxyacetic acid-stimulated elongation of pea stem segments have been investigated. A nonasaccharide (XG9) containing one fucosyl-galactosyl side chain and an undecasaccharide (XG11) containing two fucosyl-galactosyl side chains were purified from endo-beta-1,4-glucanase-treated xyloglucan, which had been isolated from soluble extracellular polysaccharides of suspension-cultured sycamore (Acerpseudoplatanus) cells and tested in the pea stem bioassay. A novel octasaccharide (XG8') was prepared by treatment of XG9 with a xyloglucan oligosaccharide-specific alpha-xylosidase from pea seedlings. XG8' was characterized and tested for its ability to inhibit auxin-induced growth. All three oligosaccharides, at a concentration of 0.1 microgram per milliliter, inhibited 2,4-dichlorophenoxyacetic acid-stimulated growth of pea stem segments. XG11 inhibited the growth to a greater extent than did XG9. Chemically synthesized nona- and pentasaccharides (XG9, XG5) inhibited 2,4-dichlorophenoxyacetic acid-stimulated elongation of pea stems to the same extent as the same oligosaccharides isolated from xyloglucan. A chemically synthesized structurally related heptasaccharide that lacked a fucosyl-galactosyl side chain did not, unlike the identical heptasaccharide isolated from xyloglucan, significantly inhibit 2,4-dichlorophenoxyacetic acid-stimulated growth.

Journal Article↗