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Biomedical subjects

S Liu

Publications and source records attributed to S Liu.

At least 919 records · Page 51Linked to original sources
PubMed1994

Effect of acceleration on the chest wall.

The gravitational force on the rib cage has been found to be an expiratory force of approximately 8 cmH2O. The gravitational force on the abdomen is an inspiratory force of the same magnitude. Because the compliance of the rib cage is greater than the compliance of the abdomen, it follows that gravity has a net expiratory effect on lung volume and that upward accelerations augmenting the gravitational force would have an additional expiratory effect. This conclusion is contrary to observations that functional residual capacity increases during headward accelerations in centrifuges and during intervals of upward acceleration in airplanes. We report the results of two studies of the effects of accelerations that are smaller in magnitude and of shorter duration than those studied in centrifuges and airplanes. The first was an experimental study of the effect of acceleration in an elevator. In subjects who relaxed against an occluded airway, airway pressure increased during upward accelerations and decreased during downward accelerations. The second was the modeling and analysis of the effects of the accelerations that occur during walking. The analysis predicted an initial expiratory response to the acceleration spike that occurs during footfall. The prediction agreed with data in the literature on the respiratory effect of walking. In both of these studies upward accelerations had an expiratory effect.

Acceleration↗
PubMed1994

Vagal stimulation induces increased pulmonary vascular permeability in guinea pig.

The effects of vagal stimulation on pulmonary vascular permeability were studied in guinea pigs in vivo using 125I-labeled albumin as a marker of plasma extravasation. Bilateral vagus nerve stimulation (NS) significantly increased the plasma leakage index in both parenchyma and tracheobronchial tissues. The NS-induced plasma leakage in the parenchyma was unaffected by the alpha-adrenoceptor antagonist phentolamine, the muscarinic receptor antagonist atropine, the ganglionic blocker hexamethonium, or pretreatment with 6-hydroxydopamine or capsaicin, but it was significantly potentiated by the beta-adrenoceptor antagonist propranolol. NS-induced tracheobronchial vascular leakage was markedly inhibited by pretreatment with atropine, hexamethonium, or capsaicin, although it was unaffected by pretreatment with phentolamine, propranolol, or 6-hydroxydopamine. By itself, NG-nitro L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthase, had no effect on pulmonary vascular leakage, but it significantly enhanced the NS-induced plasma leakage to parenchyma in a dose-related and L-arginine-reversible manner. Elevation of blood pressure to a similar extent as that induced by L-NAME by a phenylephrine infusion had no significant effect on the increased plasma leakage induced by NS. These results suggest that vagal stimulation increases plasma extravasation in lung parenchyma through the release of unidentified transmitter(s) in a process that is modulated by endogenous NO and catecholamines (via activation of beta-adrenoceptors), and that different mechanisms are involved in the vagally induced plasma extravasation in the pulmonary and tracheobronchial vascular beds.

Animals↗
PubMed1994

Cellular and molecular basis of renal repair in acute renal failure.

Experimental data suggest that the recovery of renal function after ischemic or nephrotoxic acute renal failure is due to a replicative repair process dependent on predominantly paracrine release of growth factors. These growth factors promote renal proximal tubule cell proliferation and a differentiation phase dependent on the interaction between tubule cells and basement membrane. These insights identify the molecular basis of renal repair in ischemic and nephrotoxic acute renal failure and may lead to potential therapeutic modalities that accelerate renal repair and lessen the morbidity and mortality associated with these renal disease processes.

Acute Kidney Injury↗
PubMed1994

[Causes of erroneous diagnosis in SOM].

During the years of 1988-1990, 230 ears were diagnosed as secretory otitis media (SOM), with intact data, in which 23 ears failed to be diagnosed. Atypical symptom, carelessness in collection of history and in examining the tympanic membrane were considered as one of the important causes of erroneous diagnosis. Analysis of pure tone audiogram should be combined with the age and the former history of patients. "B" type tympanograph has 88% positive rate in diagnosing SOM. So in children, acoustic impedance should be used as a routine audiometric measurements, even if with clear history of receiving ototoxic drug.

Adolescent↗
PubMed1994

[Marchiafava-Bignami disease].

One case of subacute development of Marchiafava-Bignami disease (MBD) is reported. The clinical characteristics and pathogenetic aspects of the disease are discussed. The usage of MRI in the diagnosis of MBD before the patient's death was the first ever in China.

Alcoholism↗
PubMed1994

[Influence of refined amorphophallus konjac on osteoporosis in the aged female rats: a preliminary bone histomorphometric analysis].

The hypolipidaemic and antisteatotic effects of refined amorphophallus konjac (RAK) have been reported. In order to further evaluate the effect of RAK on osteoporosis in the aged female SD rats, forty one month aged female SD rats were divided into three groups: a normal diet group (S), another normal diet group (A) and a test group (B) in which the animals were fed on a diet similar to that of the normal diet group with the addition of RAK at a dosage of 1%. At the end of the sixth month of the diet treatment, all the animals in S group were killed. Animals of the other two groups were sacrificed at the end of experiments for 18 months. Blood and right femora samples were collected for serum Ca, P, and for bone mineral contents (BMC), respectively. Inorganic matter (ash content), and calcium and phosphorus contents of the left femur were measured. Meanwhile, undecalcified sections of left tibia were processed for bone histomorphometry. The results showed that trabecular bone volume (Vv), trabecular perimeters (TRP), bone mineral contents (BMC) as well as the Ca, P contents of bone were lower in A and B than in S, but no significance was found between A and B in all of the above indices. These data exhibited: (1) Similar to the postmenopausal osteoporosis in aged women, the bone mass of the aged female rats was markedly lost in A and B. (2) A diet treatment with 1% RAK would not aggravate osteoporosis.

Animals↗
PubMed1994

[The diagnosis of primary hyperparathyroidism--analysis of 134 cases].

This article reports the diagnostic experiences of 134 cases of primary hyperparathyroidism (PHPT) confirmed by operation and pathologic examination. The clinical presentations were divided into 4 types: (1) 75 cases (56.0%) with bone resorption; (2) 47 cases (35.0%) with bone lesions plus urinary calculus; (3) 8 cases (6.0%) with urinary calculus only and; (4) 4 cases (3.0%) with hypercalcemia only. Bone lesions included bone resorption, osteomalacia and osteoporosis. Stones at multiple sites in the urinary tract or nephrocalcinosis were found in 41 cases. The measurement of ionized calcium was much more sensitive and accurate than the total calcium assay with the positive rate of 95.3% and 73.4% respectively. The concentration of plasma iPTH was high in the whole group (n = 84), the mean value was 21.4 +/- 17.9 times higher than that of the normal control group. For the localization of the affected parathyroid gland, instiat examination was by neck ultrasonography which gone a positive predictive value of 81.5% (43/53), 99mTc-MIBI scan showed positive rate 94.1% (16/17). The CT scan of the chest was used when ectopic location in mediastinum was highly suspected. If the first operative exploration failed to find the affected parathyroid gland, we performed the determinations of iPTH with samples taken from internal jugular vein through selective venous catheterization; the coincidence rate was found to be 85.2% (23/27).

Adenocarcinoma↗
PubMed1994

[Effects of zuzhongping on ischemic volume in the rat model of middle cerebral artery occlusion].

Using the middle cerebral artery occlusion model, we studied the effects of Zuzhongping on experimental focal cerebral ischemia. Twenty-eight adult male Wistar rats were randomly divided into three groups: (1) Zuzhongping group (n = 9), (2) Saline control group (n = 10), and (3) Blank control group (n = 9). Group 1 and group 2 received via a gastric tube 1 1ml/kg/day of Zuzhongping and normal saline, respectively. The cerebral middle arteries on the right side of 28 rats were occluded with a bipolar electro-coagulater at sites 1-2 mm from the right olfactory nerve tract. Ischemic volumes were measured by an image analytic system when the cerebral ischemia had lasted 24 h. The results showed that the ischemic volume of Zuzhongping group was significantly smaller than that of group 2 and group 3, suggesting a protective effect of Zuzhongping.

Animals↗
PubMed1994

[Amplification of C-myc oncogene in squamous cell carcinoma of the larynx].

C-myc amplification in 22 squamous cell carcinomas and 10 normal tissues (control) from the larynx was assessed by dot hybridization technique. Significant amplification of C-myc oncogene was found in malignant tumours as compared with the normal tissues. The extent of amplification also correlated with advanced tumour stages. There was a significant increase in C-myc amplification in TNM stages III and IV when compared with the stages I and II. These data suggested that C-myc oncogene might be activated by gene amplification and it might have a key role in determining the aggressiveness of laryngeal carcinoma.

Carcinoma, Squamous Cell↗
PubMed1994

Nuclear-encoded mitochondrial precursor protein: intramitochondrial delivery to dendrites and axon terminals of neurons and regulation by neuronal activity.

Mitochondria contain hundreds of proteins, most of which are encoded by the nucleus. In neurons, distal dendrites and axon terminals can be separated from the nucleus by a great distance, and the mechanism by which precursor proteins reach distal neuronal processes is not well understood. While our previous study on cytochrome oxidase suggests a post-translational mechanism of delivery, it is not known whether precursor proteins reach their target processes before or after incorporation into mitochondria. In order to localize only precursor proteins and not the mature form of the subunit in neurons, we generated polyclonal antibodies against synthetic presequence polypeptides specific to nuclear-encoded subunit IV precursor protein of rat brain cytochrome oxidase. We found that the precursors were located not only in neuronal cell bodies, but also in dendrites and axon terminals. This indicates that the conversion of these precursors to their mature form is not confined to the cell body but occurs in dendrites and axons as well. At the electron microscopic level, an overwhelming majority of immunoreaction product was found within mitochondria, suggesting that precursor proteins are transported to neuronal processes mainly within mitochondria, and that their half-lives are much longer in neurons than in yeast and rat hepatocytes. The precursor pool was downregulated in the rat superior colliculus after monocular enucleation, indicating that precursor synthesis and/or degradation is regulated by neuronal functional activity. These results also suggest that local functional demands may play an important role in controlling the processing of precursors and the assembly of holoenzymes in dendrites and axon terminals. This allows neurons to regulate enzyme levels locally, precisely, and rapidly.

Animals↗
PubMed1994

Peroxynitrite, a product of superoxide and nitric oxide, produces coronary vasorelaxation in dogs.

The vascular effect of peroxynitrite (ONOO-), a product of superoxide anion and nitric oxide, in isolated canine coronary arteries bathed in a 10 mM 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid-buffered physiological salt solution (pH 7.4) was investigated. ONOO- was synthesized from nitrite and H2O2 in a quenched-flow reactor. Addition of 0.01 to 30 microM ONOO- produced a rapid, dose-dependent relaxation in all 17 rings of coronary arteries with a threshold concentration of 0.1 microM, IC50 of 1.0 +/- 0.1 microM and Emax of -96 +/- 0.5% (Means +/- S.E.M.). Incubation of arteries in a standard bicarbonate-buffered Krebs-Henseleit solution decreased slightly the sensitivity of ONOO- relaxation but did not alter the maximum effect (Emax = -97 +/- 1.1, n = 6 vessels). The ONOO(-)-induced coronary relaxation was reversible upon washing, and was also reproducible with repeated testings in the same ring. Mechanical removal of intimal endothelium did not alter the observed relaxant effect. Addition of superoxide dismutase (100 U/ml) potentiated the ONOO- relaxation by shifting the dose-response curve to the left (IC50 = 0.4 +/- 0.1 microM, P < .05, n = 17), whereas 3 microM hemoglobin inhibited it by shifting the curve to the right (IC50 = 20 +/- 4 microM, P < .05, n = 15). Relaxation was also observed with higher concentrations of sodium nitrite and decomposed ONOO-, although the time course of the development of these relaxations was considerably slower and with reduced sensitivity. In addition, superoxide dismutase had no effect on the latter relaxation responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

The contribution of intermolecular hydrogen bonding to the kinetic specificity of papain.

The binding of substrates to the active site of papain is thought to involve, among other things, intermolecular P1NH-OC(Asp158) and P2NH-OC(Gly66) hydrogen bonding. In this study the contribution of these two putative hydrogen bonds to the interaction specificity of papain was measured for pairs of ligands in which the amide NH in question was either intact or replaced by an ester O linkage. The probe ligands investigated comprised substrates (peptidyl p-nitroanilides), substrate-like transition state analog inhibitors (peptidyl nitriles) and substrate-like affinity labeling agents (peptidyl Michael acceptors). Observed differences in interaction energies (delta delta G(obs) or delta delta G(obs) not equal to) for amide/ester ligand pairs indicated an apparent specificity energy of 2.1-2.6 kcal/mol for the P2NH-OC(Gly66) bond. For the P1NH-OC(Asp158) bond delta delta G(obs) was approx. 1.0 kcal/mol for dipeptidyl ligands but close to zero for ligands lacking a P2NH donor. These specificity energies are comparable to values reported for other enzyme-ligand systems. However, the dependence of delta delta G(obs) for the P1NH-OC(Asp158) bond on the presence of a P2NH donor suggests that these two hydrogen bonds may interact cooperatively in ligand binding. A thermodynamic cycle approach was used to relate delta delta G(obs) to actual hydrogen bond strengths and other aspects of enzyme-ligand and solvent-ligand interactions.

Amino Acid Sequence↗
PubMed1993

Lipopolysaccharide treatment in vivo induces widespread tissue expression of inducible nitric oxide synthase mRNA.

Nitric oxide (NO) may mediate the hypotension of septic shock, but the effect of endotoxin on inducible NO synthase (iNOS) mRNA expression remains unclear. We studied the effects of lipopolysaccharide (LPS) treatment in vivo on iNOS mRNA expression using reverse transcription and polymerase chain reaction. The iNOS mRNA was absent or negligible in any tissue studied from control rats, but was markedly increased in lung, liver, spleen, skeletal muscle and kidney from LPS-treated rats. The LPS-induced increase in iNOS mRNA was prevented by dexamethasone. Our results indicate that LPS treatment in vivo induces the expression of an iNOS mRNA via a dexamethasone-sensitive mechanism, and thus provide direct molecular evidence for the involvement of NO in septic shock.

Amino Acid Oxidoreductases↗
PubMed1993

Cloning, expression and mutational analysis of SH-PTP2, human protein-tyrosine phosphatase.

A human cDNA clone encoding a nonreceptor protein-tyrosine-phosphatase (PTP) has been isolated and sequenced. The 2.1 kilobase pair cDNA encodes for a 593 amino acid protein that contains a single tyrosine phosphatase catalytic domain at the C-terminus. At the N-terminus the protein has two adjacent copies of Src homology region (SH2 domain) which show 61% and 73% identity at the amino acid level to the SH2 domains of the human PTP1C and Drosophila corkscrew protein, respectively. The overall homology between SH-PTP2 and PTP1C or to corkscrew protein is 58%. When this protein (or its catalytic domain) was expressed in E. coli as a glutathione-S-transferase fusion protein tyrosine-phosphatase activity was detected in bacterial cell extracts. Site-directed mutation made at the conserved cysteine (459) residue to serine within the highly conserved VHCXAGXXR sequence in the PTP catalytic domain resulted in complete loss of enzymatic activity demonstrating the importance of this cysteine residue in catalysis. Northern blot analysis showed that SH-PTP2 is expressed as a 6.5 kilobase mRNA in a number of fetal and adult human tissues and cell lines. The highest levels of its mRNA were detected in fetal brain and in adult heart tissue. The identification of SH-PTP2 along with PTP1C and corkscrew protein suggest that there exist a family of nonreceptor PTP containing SH2-domain which will participate in specific signal transduction pathways involving tyrosine phosphorylation-dephosphorylation.

Amino Acid Sequence↗
PubMed1993

Expression of an EF-1 alpha-like rat cDNA, S1, in E. coli and production of a rabbit polyclonal antiserum to the recombinant protein.

A previously identified rat cDNA (S1) that shares 78% nucleotide homology and a predicted 92% amino acid homology with human EF-1 alpha was constructed into PGEX-2T and inducibly expressed in E. coli as a fusion protein. The purified recombinant S1 protein (rpS1) was used to raise rabbit antiserum which recognized rpS1 but not EF-1 alpha on immunoblots. A polyclonal antiserum to EF-1 alpha failed to react with the rpS1. Our results indicate that rpS1 protein can be used to produce antibodies which distinguish pS1 from EF-1 alpha despite their extensive amino acid sequence homology.

Amino Acid Sequence↗
PubMed1993

Mechanism of inactivation of S-adenosylhomocysteine hydrolase by (Z)-4',5'-didehydro-5'-deoxy-5'-fluoroadenosine.

S-Adenosyl-L-homocysteine (AdoHcy) hydrolase, an enzyme important in the regulation of biological methylation reactions, was shown by McCarthy et al. (McCarthy, J.R., Jarvi, E.T., Matthews, D.P., Edwards, M.L., Prakash, N.J., Bowlin, T.L., Mehdi, S., and Bey, P. (1989) J. Am. Chem. Soc. 111, 1127-1128) to be inactivated by (Z)-4',5'-didehydro-5'-deoxy-5'-fluoroadenosine (ZDDFA). In this study we have shown that the mechanism of this inactivation of AdoHcy hydrolase (NAD+ form) includes a rapid addition of water to the 5'-position of ZDDFA and elimination of fluoride ion, resulting in the formation of the 5'-carboxaldehydes 3 and 4. The 5'-carboxaldehydes 3 and 4 are then oxidized in a slower step to the 3'-keto-5'-carboxaldehydes 5 and 6 by reduction of the enzyme-bound NAD+ to NADH. Evidence in support of this mechanism includes the observation that the first step in this mechanism (i.e. elimination of fluoride ion and formation of the 5'-carboxaldehydes 3 and 4) can be catalyzed by apo-AdoHcy hydrolase and the NADH form of AdoHcy hydrolase. Incubation of ZDDFA with either the apo or NADH form of AdoHcy hydrolase resulted in rapid release of fluoride ion (determined by 19F NMR) and formation of the 5'-carboxyaldehydes 3 and 4 (determined by high performance liquid chromatography). The carboxaldehydes 3 and 4 were synthesized independently and were shown to be potent inhibitors of the NAD+ form of the enzyme. When the relative first-order rates of fluoride ion release (determined by 19F NMR) from ZDDFA, NAD+ reduction to NADH, and inactivation of the NAD+ form of the enzyme were compared, the release of fluoride ion was found to be approximately 20 times faster than NAD+ reduction or enzyme inactivation. Incubation of ZDDFA with the NAD+ form of AdoHcy hydrolase was shown to afford the 3'-keto-5'-carboxaldehydes 5 and 6, which were also formed upon incubation of the enzyme with the 5'-carboxaldehydes 3 and 4. The 3'-keto-5'-carboxaldehydes 5 and 6 were shown to be tightly (but not covalently) bound to the enzyme, since these products could be released by treatment of the ZDDFA-inactivated enzyme with HClO4 or other denaturing agents.

Adenosine↗