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Biomedical subjects

L Yu

Publications and source records attributed to L Yu.

At least 163 records · Page 9Linked to original sources
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

Sucrase-isomaltase gene expression along crypt-villus axis of human small intestine is regulated at level of mRNA abundance.

The mucosal lining of the small intestine is a complex epithelium that is continually renewed by division of a stem cell population located in intestinal crypts, migration of daughter cells along the villus, and, finally, extrusion of senescent cells into the lumen. The majority of cells in both crypt and villus cell compartments are enterocytes that acquire differentiated functions as they migrate out of the crypt. Sucrase-isomaltase (SI) is an enterocyte-specific, brush-border enzyme that has little activity in crypt cells and maximal activity in low and mid villus cells. The mechanism by which enterocytes acquire SI enzymatic activity as they move from crypt to villus is controversial. In this study we examined the distribution of SI mRNA along the crypt-villus axis of human small intestine using isolated epithelial cells and in situ hybridization. A complementary DNA to the 5' portion of the human SI mRNA was amplified and cloned using the polymerase chain reaction. Hybridization analysis of RNA extracted from human intestinal epithelial cells showed that the cloned cDNA recognized a single 6.5-kb mRNA. In situ hybridization of duodenal biopsy specimens was performed using a single-stranded RNA probe derived from this cDNA. This analysis showed that there was little SI mRNA in crypt cells and appearance of mRNA in enterocytes located at the crypt-villus junction. The mRNA levels were maximal in lower and mid villus cells with decreased levels noted in villus tip cells. These results are identical to those previously described in rat intestine and suggest that expression of the SI gene as enterocytes emerge from intestinal crypts is regulated primarily at the level of mRNA accumulation. Study of SI gene regulation may provide a useful model to investigate the mechanisms that regulate enterocyte-specific gene expression and intestinal differentiation.

Amino Acid Sequence↗
PubMed1992

Differential regulation of cytochrome P-450 genes along rat intestinal crypt-villus axis.

Mammalian small intestine contains cytochrome P-450-dependent monooxygenase enzymes that are capable of metabolizing a wide variety of xenobiotics and activating procarcinogens to mutagenic compounds. The epithelial cells lining the small intestine are separated into a proliferating undifferentiated compartment located in crypts and a nonproliferating differentiated compartment located on villi. The constitutive expression and induction by xenobiotics of genes that encode components of the cytochrome P-450-dependent mono-oxygenase system along the rat intestinal crypt-villus axis were investigated using isolated epithelial cells and in situ hybridization. For each gene examined, hybridization analysis of RNA obtained from isolated epithelial cells correlated with findings on in situ RNA hybridization. Cytochrome P-450IA1 mRNA (CYP1A1), the major aromatic hydrocarbon-inducible P-450, and cytochrome P-450IIB1 mRNA (CYP2B1), the major phenobarbital-inducible P-450, were constitutively expressed in villus cells with no detectable mRNA present in crypts. Treatment with several chemical inducers resulted in a marked increase in CYP1A1 mRNA in both crypt and villus cells. In contrast, although CYP2B1 mRNA was inducible in villus cells, CYP2B1 mRNA was not detected in crypts after treatment with chemical inducers. NADPH cytochrome P-450 reductase, a necessary component for the activity of all P-450 enzymes, was expressed constitutively at low levels only in villus cells. Treatment with dexamethasone induced reductase mRNA in both crypt and villus cells. Taken together, these results demonstrate that there is a complex gene-specific pattern of expression of the microsomal monooxygenase system along the crypt-villus axis of rat small intestine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Acute renal failure following hemorrhagic shock: protective and aggravating factors.

Acute renal failure following hemorrhagic shock was studied in awake rats. The animals were bled to maintain the mean arterial blood pressure between 40 and 60 mm Hg during 180 min. After this period, the blood was reinfused and the rats were studied 24 h later. Hemorrhagic shock caused a less intensive renal injury than 60-min bilateral renal artery clamping. Renal function in the latter model was worse (p less than 0.05) as shown by serum creatinine (SCr) (0.75 +/- 0.10 vs 1.2 +/- 0.2 mg/dL), blood urea nitrogen (BUN) (26.0 +/- 2.8 vs 53.0 +/- 8.5 mg/dL), fractional excretion of sodium (FENa, %) (0.3 +/- 0.1 vs 1.8 +/- 1.0) and potassium (FEK, %) (41.4 +/- 5.7 vs 76.3 +/- 14.2) and urine/plasma creatine (U/PCr (86.4 +/- 15.7 vs 38.8 +/- 15.5). The rats which received verapamil (10 micrograms/kg/min) prior and during the HS did not show increase in SCr (0.5 +/- 0.06 vs 0.75 +/- 0.1 mg/dL, p less than 0.05). This effect was also observed in the rats which received intravenous allopurinol (40 mg/kg) before HS, SCr did not increase (0.5 +/- 0.04 vs 0.75 +/- 0.1 mg/dL, p = 0.05), suggesting a protective effect of those substances in HS.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1992

Late evaluation of glomerular filtration rate, proteinuria, and urinary acidification after acute tubular necrosis.

Fourteen patients were studied 2 to 36 months after acute tubular necrosis. It was observed that 43% of the patients had decreased glomerular filtration rate. These patients were older and had lower urinary excretion of ammonium and titratable acidity. Proteinuria greater than 150 mg/day, without reaching a nephrotic level, was found in 92% of the patients. The presence of oliguria, the demand of dialysis, and the acute tubular necrosis etiology were not statistically different among the patients who recovered their glomerular filtration rate either totally or partially.

Adult↗
PubMed1992

[Preliminary study on RFLPs for dystrophin gene in Chinese].

We have studied the RFLPs distribution and frequency of dystrophin gene in Chinese by using 14 subclones of complete 14 kb cDNA for the dystrophin gene as hybridization probes. Allelic fragments are detected in hybridization patterns of Pvu II/1a, Taq I/2b-3, Taq I/5b-7, Xba I/10. Among them, the allelic fragments (26 kb and 3.8 kb) in Pvu II/2b-3 patterns and the allelic fragments (10 kb and 8.4 kb) in Taq I/5b-7 patterns are the new RFLPs which have never been reported. From the comparison of our data with those of Caucasian and Japanese respectively and their statistical analysis, we can obtain the results as follows: There is remarkable difference (p less than 0.01) of the allelic fragment frequency in Taq I/2 b-3 (A1 = 3.4 kb, fre. 0.04; A2 = 3.2 kb, fre. 0.96) and Xba I/10 (A1 = 7.4 kb, fre. 0.41; A2 = 6.7 kb, fre. 0.59) between Chinese and Caucasian. The frequency of the allelic fragments A2 in Taq I/8 (A1 = 6.5 kb, A2 = 5.6 kb) and EcoR V/9 (A1 = 11.8 kb, A2 = 10.7 kb) are high in Caucasian, but have not been detected in Chinese. These differences are also highly significant. But the B1B2 allelic frequencies in Taq I/5 b-7 (B1 = 3.2 kb, B2 = 1.6 kb) are the same. There is no significant difference in the frequency of the allelic fragments A1A2 and B1B2 in Pvu II/1 a between Chinese and Japanese. Preliminary results suggest that there probably are high frequencies for spontaneous neutral mutations in the evolution process of the huge dystrophin gene (about 2,300 kb). In the meantime, the neutral mutation frequencies of various sectional sequences have remarkable differences, and that of some sectional sequences of the gene between Chinese and Caucasian may also have remarkable differences.

Adult↗
PubMed1992

[Effect of 764-3 on bleomycin activation of alveolar macrophages].

The effect of pretreatment with 764-3, a huo xue hua yu medicine, on bleomycin A6 activation of alveolar macrophages of rats was observed. Results showed that bleomycin A6 could activate alveolar macrophages directly and that 764-3 could inhibit the activating effect of bleomycin A6. When alveolar macrophages are activated, they release not only PMN chemotactic factor, but also many destructive lysosomal enzymes, superoxide anions, etc, possibly resulting in serious injury to the lungs.

Animals↗