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Biomedical subjects

H Q Zhou

Publications and source records attributed to H Q Zhou.

8 recordsLinked to original sources

[Detection of plasma urokinase-type plasminogen activator and its receptor in acute or chronic hepatitis B patients and its clinical significance.].

BACKGROUND: To study the expression of plasma uPA and uPAR in Acute or Chronic Hepatitis B patients, to investigate changes of blood fibrinolytic system in Hepatitis B and its clinical significance. METHODS: The level of detected plasma urokinase-type plasminogen activator (uPA) and urokinase-type plasminogen activator receptor (uPAR) were measured by Enzyme Linked Immuno Sorbent Assay (ELISA). RESULTS: The levels of plasma uPA and uPAR were significantly higher in patients with Acute or Chronic Hepatitis B than that of control group (P less than 0.05, P less than 0.01), and also higher in serious group than that of non-serious group of Chronic Hepatitis B patients (P less than 0.05), and also higher in chronic group than in acute group (P less than 0.05). The level of plasma uPAR was significantly higher in patients with serious jaundice than that of non-serious jaundice group (P less than 0.01). The levels of uPA and uPAR are significantly higher in acute period than that in recover period of Acute Hepatitis B patients, but the levels in recover period is also higher than that in control group. The level of plasma uPAR have positive correlation with prothrombin (PT), international normalized ratio (INR) and total bilirubin (P less than 0.01). CONCLUSION: The level of plasma UPA nad UPAR were enhanced in Acute or Chronic Hepatitis B patients was related with the degree of inflammation, was also related with high expression of serious damage of liver cell. It may be one of important cause to imbalance between coagulation and fibrinolytic in hepatitis.

Hepatitis B↗

Studies on the inactivation of bovine liver enoyl-CoA hydratase by (methylenecyclopropyl)formyl-CoA: elucidation of the inactivation mechanism and identification of cysteine-114 as the entrapped nucleophile.

The inhibitory properties of (methylenecyclopropyl)formyl-CoA (MCPF-CoA), a metabolite derived from a natural amino acid, (methylenecyclopropyl)glycine, against bovine liver enoyl-CoA hydratase (ECH) were characterized. We have previously demonstrated that MCPF-CoA specifically targets ECHs, which catalyze the reversible hydration of alpha,beta-unsaturated enoyl-CoA substrates to the corresponding beta-hydroxyacyl-CoA products. Here, we synthesized (R)- and (S)-diastereomers of MCPF-CoA to examine the stereoselectivity of this inactivation. Both compounds were shown to be competent inhibitors for bovine liver ECH with nearly identical second-order inactivation rate constants (k(inact)/K(I)) and partition ratios (k(cat)/k(inact)), indicating that the inactivation is nonstereospecific with respect to ring cleavage. The inhibitor, upon incubation with bovine liver ECH, labels a tryptic peptide, ALGGGXEL, near the active site of the protein, where X is the amino acid that is covalently modified. Cloning and sequence analysis of bovine liver ECH gene revealed the identity of the amino acid residue entrapped by MCPF-CoA as Cys-114 (mature sequence numbering). On the basis of gHMQC (gradient heteronuclear multiple quantum coherence) analysis with [3-(13)C]-labeled MCPF-CoA, the ring cleavage is most likely induced by the nucleophilic attack at the terminal carbon of the exomethylene group (C(2)'). We propose a plausible inactivation mechanism that involves relief of ring strain and is consistent with examples found in the literature. In addition, these studies provide important clues for future design of more efficient and selective inhibitors to control and/or regulate fatty acid metabolism.

Acyl Coenzyme A↗

Ladder operator for the one-dimensional Hubbard model.

The one-dimensional Hubbard model is integrable in the sense that it has an infinite family of conserved currents. We explicitly construct a ladder operator which can be used to iteratively generate all of the conserved current operators. This construction is different from that used for Lorentz invariant systems such as the Heisenberg model. The Hubbard model is not Lorentz invariant, due to the separation of spin and charge excitations. The ladder operator is obtained by a very general formalism which is applicable to any model that can be derived from a solution of the Yang-Baxter equation.

Journal Article↗

4-aminopyridine, a specific blocker of K(+) channels, inhibited inward Na(+) current in rat cerebellar granule cells.

The effects of 4-aminopyridine (4-AP), a specific blocker of outward K(+) current, on voltage-activated transient outward K(+) current (I(K(A))) and inward Na(+) current (I(Na)) were investigated on cultured rat cerebellar granule cells using the whole cell voltage-clamp technique. At the concentration of 1-5 mM, 4-AP inhibited both I(K(A)) and I(Na). It reduced the amplitude of peak Na(+) current without significant alteration of the steady-state activation and inactivation properties. The inhibitory effect was not enhanced by repeated depolarizing pulses (0.5 or 0.1 Hz), suggesting that the binding affinity of 4-AP on Na(+) channels is state-independent. In contrast, the effect of 4-AP on Na(+) channels appeared to be voltage-dependent, the weaker inhibition occurred at more depolarization. Moreover, 4-AP slowed both the activation and inactivation kinetics of Na(+) current. These effects were similar to those induced by alpha-scorpion toxin and sea anemone toxins on Na(+) channels in other cell model. Our data demonstrate for the first time that 4-AP is able to block not only A-type K(+) channels, but also Na(+) channels in rat cerebellar granule cells. It is concluded that the inhibition exerted by 4-AP on Na(+) current likely differs from that provoked by local anesthetics. The possibility that the binding site of neurotoxin receptor 3 may be involved is discussed.

4-Aminopyridine↗

The abnormality of glucose transporter in the erythrocyte membrane of Chinese type 2 diabetic patients.

Type 2 diabetes mellitus is characterized by impaired glucose uptake. With a photometric method of recording the erythrocyte suspension absorption during the course of glucose transport across the membranes, we observed that the initial rate of glucose zero-trans entry was decreased significantly in 30 Chinese type 2 diabetic patients as compared to 25 healthy controls. The rate of glucose infinite-cis efflux exhibited no difference between the patients and controls. The measurement of temperature dependence of glucose transport showed that the activation energy for glucose entry was increased in diabetic patients. The inhibitory constant of glucose entry by cytochalasin B (CB) in patients was similar to that of the controls. However, we found that the inhibitory constant was increased significantly in the patient erythrocytes after phloretin treatment. After the erythrocytes were made into stripped white ghosts, the fluorescence quenching experiment was performed. Glucose, CB and phloretin can quench the fluorescence of tryptophan residues in the glucose transporter 1, GLUT1. The abnormality of fluorescence quenching in the erythrocyte membranes of patients was observed. The transfer tendency of tryptophan residues from the hydrophilic environment to the hydrophobic environment was decreased in patient ghosts as binding with glucose, and the opposite tendency appeared as CB and phloretin instead of glucose. We conclude that the decreased in glucose entry in the erythrocyte membranes of diabetic patients was due to the GLUT1 change in structure - mostly the outer domain of the glucose transporter.

Asian People↗

Swelling-activated chloride currents in embryonic chick heart cells.

AIM: To characterize a swelling-activated chloride current, I(Cl, swell), in white Leghorn chick heart cells and the effects of chlorpromazine (CPZ) effects. METHODS: The patch-clamp technique in the whole-cell configuration was used. RESULTS: Hyposmotic swelling elicited I(Cl, swell) in white Leghorn chick heart cells. The current amplitude increased from (452 +/- 200) pA to (849 +/- 373) pA with a reduction of osmolarity from 300 mmol.L-1 to 270 mmol.L-1, 4',4-Diisothiocyanostilbene-2,2'-disulphonic acid (DIDS) 100 mumol.L-1 decreased I(Cl, swell) from (1196 +/- 505) pA to (830 +/- 328) pA in hyposmotic solution. In white Leghorn chick heart cells I(Cl, swell) was not induced by CPZ 30 mumol.L-1, which is different from the case of E coli spheroplast. CONCLUSION: Swelling-activated chloride current was activated by hyposmotic swelling in white Leghorn chick heart cells. The mechanism for activating the current is different from that of mechanosensitive ion channels of E coli.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

Characterization of outward potassium current in embryonic chick heart cells.

AIM: To characterize a voltage-dependent outward K+ current in cultured heart cells of 14-16-day-old embryos of yellow chick. METHODS: The patchclamp technique in the whole-cell configuration was used. RESULTS: The kinetics and the pharmacology of the outward K+ current in our cell mold were different from those described in white chick. Like the calcium-activated K+ current, blocker of calcium channel, CdCl2, eliminated the current of more than 95%. Isoproterenol provoked an increase of peak amplitude (137% +/- 47%, n = 16 cells) and acceleration of activation kinetics in the outward K+ current (the time reaching a peak current reduced from 36 ms +/- 10 ms to 16 ms +/- 9 ms). This effect of isoproterenol was mimiced by cAMP. In addition, a frequency-dependent decrease in peak amplitude of the current occurred after cAMP-induced phosphorylation. CONCLUSION: There are species- and/or cell-type-specific difference in the K+ channels properties. In embryonic yellow chick heart cells, the phospholation of channel could not only modulate the activation kinetic properties of the calcium-activated potassium channel, but also change their recovery kinetics.

Animals↗