Biomedical subjects

Liang Zhao

Publications and source records attributed to Liang Zhao.

59 records · Page 4Linked to original sources

PubMed2002

Primate neurons show different vulnerability to transient ischemia and response to cathepsin inhibition.

Previously, we reported "calpain-induced leakage of lysosomal enzyme cathepsin" as a mechanism of ischemic neuronal death specific for primates. Cathepsin inhibitors such as CA-074 and E-64c were demonstrated to significantly inhibit hippocampal neuronal death. Pyramidal neurons of the hippocampus, Purkinje cells in the cerebellum, and neurons in the caudate nucleus, outer putamen and cortical III, V layers, are known to be vulnerable to ischemia. However, regional differences of the vulnerability and response to neuroprotectants, have not been studied in detail. Here, the monkey brains undergoing transient ischemia were studied to clarify such regional differences by the microscopic counting of surviving neurons. The dead neurons were characterized by eosinophilic coagulation necrosis without apoptotic bodies. The control postischemic brain without treatment showed surviving neurons in caudate nucleus (55.8%), outer putamen (44.4%), cortical III layer (37.8%), CA4 (35.3%), cortical V layer (34.1%), cerebellum (28.2%), CA3 (24.3%), CA2 (16.2%), and CA1 (2.0%). Only the CA1 showed an almost total neuronal loss. In contrast, a single postictal injection of CA-074 or E-64c led to significant inhibition of postischemic neuronal death in all brain regions studied. Overall, more surviving neurons were seen after E-64c treatment than with CA-074: cerebellum, 91.6% vs 85.6%; CA4, 88.6% vs 77.3%; caudate nucleus, 86.1% vs 89.8%; CA2, 83.6% vs 53.0%; outer putamen, 81.3% vs 87.7%; CA1, 80.1% vs 47.4%; CA3, 79.6% vs 60.3%; cortical layer III, 75.5% vs 67.7%; and cortical layer V, 75.0% vs 65.9%, for E-64c and CA-074, respectively. Cathepsin plays a critical role in ischemic neuronal death, and its inhibitors may protect neurons throughout the brain.

Animals↗

PubMed2002

[Annual cycle and budgets of nutrients in the Bohai Sea].

High concentrations of dissolved inorganic nitrogen and phosphate contributed much to the environmental problems in the Bohai Sea in the last decade. It is important to understand the cycle and the budget of nutrients for the environmental management. A three-dimensional ecosystem model, coupled with a physical transport model, was adopted in this study. The simulation of the year 1982 was validated by data in 1982/1983. There were depletion from spring to summer and elevation from autumn to winter for nutrients. The higher concentration of phosphate was found at the Bohai Bay and the concentration of phosphate maintained higher level in the whole year. The higher concentration of dissolved inorganic nitrogen located near the Huanghe Estuary. Production and respiration were the most important sink and source of nutrients. The remineralization of the detritus pool can compensate 30 percent of the consumption of nutrient by the production process. The inputs of phosphates and nitrogen from river were P 0.55 x 10(3) t and N 52.7 x 10(3) t.

Animals↗

PubMed2002

PET imaging of ischemic neuronal death in the hippocampus of living monkeys.

The aim of the present study was to visualize postischemic hippocampal neuronal death in the living monkey brain, using a high-resolution positron emission tomography (PET) and novel radioligands. In preceding papers, we reported on postischemic hippocampal neuronal death in a model of Japanese monkeys (Macaca fuscata) undergoing a 20-min complete whole-brain ischemia. Using the same model here, we investigated the in vivo bindings of two radiotracers, [11C]Ro15-4513 (a type II benzodiazepine receptor ligand) and [11C](+)3-MPB (a muscarinic cholinergic receptor ligand), in the hippocampus on day 7 after ischemia, as compared to the normal hippocampus. A significant decrease in the in vivo binding of [11C]Ro154513 and [11C(+)3-MPB was observed in the postischemic monkey hippocampus on day 7 after ischemia compared to controls. Light and electron microscopic analyses of postischemic CA1 neurons showed typical features of coagulation necrosis, as associated with a marked reduction of postsynaptic densities and presynaptic vesicles. These results suggest that semiquantification of hippocampal neuronal death is possible in the living primate brain using PET, and that the same procedures can be applied for evaluating neuronal cell loss in patients with ischemic injuries and/or dementia.

Affinity Labels↗

PubMed2002

[Preparation of polymer modified stationary phases through surface radical chain transfer reaction].

It is demonstrated that radical chain transfer to thiol-terminated self-assembled monolayer and surface-initiated polymerization could be used for in-situ grafting ultra-thin polymer film on silica. The widely used silane coupling agent mercaptopropyltrimethoxysilane (MPS) was used to prepare the thiol-terminated silica, and in the presence of which, chain-transfer reaction and polymerization of methyl methacrylate (MMA) was carried out using azo di-isobutylnitrile (AIBN) as the initiator. Both thiol-terminated silica and polymer film modified silica were characterized by Fourier transform infrared spectroscopy (FTIR), Raman spectroscopy, thermogravimetric analysis (TGA) and elemental analysis. The results showed that the grafting amount of polymer on silica was higher than the traditional methods, which can effectively relieve the non-specific adsorption of solute with uncovered hydroxyl groups on the surfaces of silica in subsequent chromatographic application. The obtained polymethylmethacrylate (PMMA) modified silica exhibited excellent separation capacity on the separation of the polar compounds and polycyclic aromatic hydrocarbons. This kind of surface initiated polymerization prospects for the preparation of polymer modified stationary phases.

English Abstract↗

PubMedDate not supplied

Molecular interaction between organophosphorus acid anhydrolase and diisopropylfluorophosphate.

Organophosphorus acid anhydrolases (OPAA; E.C.3.1.8.2) are a class of enzymes that hydrolyze a variety of toxic acetylcholinesterase-inhibiting organophosphorus (OP) compounds, including pesticides and fluorine-containing chemical nerve agents. In this paper, subphase conditions have been optimized to obtain stable OPAA Langmuir films, and the diisopropylfluorophosphate (DFP) hydrolysis reaction catalyzed by OPAA in aqueous solution and at the air-water interface was studied. OPAA-DFP interactions were investigated utilizing different spectroscopic techniques, that is, circular dichroism and fluorescence in aqueous solution and infrared reflection absorption spectroscopies at the air-water interface. The characterization of OPAA and its secondary structure in aqueous solution and as a monolayer at the air-water interface in the absence and in the presence of DFP dissolved in aqueous solution or in the aqueous subphase demonstrated significantly distinctive features. The research described herein demonstrated that OPAA can be used in an enzyme-based biosensor for DFP detection.

Aryldialkylphosphatase↗