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Biomedical subjects

Z H Lu

Publications and source records attributed to Z H Lu.

60 records · Page 4Linked to original sources
PubMed1990

Molecular characterization of a rat alpha 2B-adrenergic receptor.

Alpha 2-adrenergic receptors comprise a heterogeneous population based on pharmacologic and molecular evidence. We have isolated a cDNA clone (pRNG alpha 2) encoding a rat alpha 2-adrenergic receptor. A rat kidney cDNA library was screened with an oligonucleotide complementary to a highly conserved region found in all biogenic amine receptors described to date. The deduced amino acid sequence displays many features of guanyl nucleotide-binding protein-coupled receptors except it does not have a consensus N-linked glycosylation site near the amino terminus. Membranes prepared from COS cells transfected with pRNG alpha 2 DNA display high affinity and saturable binding to [3H]rauwolscine (Kd = 2 nM). Competition curve data analysis shows that RNG alpha 2 protein binds to a variety of adrenergic drugs with the following rank order of potency: yohimbine greater than or equal to chlorpromazine greater than or equal to prazosin greater than or equal to clonidine greater than norepinephrine greater than or equal to oxymetazoline. RNG alpha 2 RNA accumulates in both rat kidney and neonatal rat lung (predominant species is 4000 nucleotides). When a cysteine residue (Cys-169) that is conserved among all members of the seven-transmembrane-region superfamily is changed to phenylalanine, the RNG alpha 2 protein fails to bind [3H]rauwolscine after expression in COS cells. We conclude that pRNG alpha 2 likely represents a cDNA for a rat alpha 2B-adrenergic receptor.

Animals↗
PubMed1990

Gangliosides stimulate calcium flux in neuro-2A cells and require exogenous calcium for neuritogenesis.

The neuritogenic effect of exogenous ganglioside has been documented with a variety of neuronal and neuroblastoma systems, but the mechanism is not understood. Involvement of Ca2+ is suggested by this study which demonstrates that treatment of Neuro-2A cells with bovine brain gangliosides (BBG) in Ca2(+)-depleted medium failed to produce neurite outgrowth. This was in contrast to treatment with retinoic acid or dibutyryl cyclic AMP which induced differentiation under the same conditions. Addition of BBG to Neuro-2A cells caused small, but significant, increases in both influx and efflux of Ca2+. It thus appears that although neuritogenesis can proceed by more than one mechanism, that induced by BBG requires exogenous Ca2+ and involves stimulation of Ca2+ flux.

Animals↗
PubMed1989

[An experimental study on the contents of enkephalins in the cerebrospinal fluid in rabbits with unilateral destructive lesions produced in the substantia nigra and their relation to the regulation of MIF-1].

The changes of the contents of enkephalins in cerebrospinal fluid (CSF) and the action of MIF-1 in rabbit experimental models of Parkinson's disease were studied. In the experiment, the rabbits received injection of 6-hydroxydopamine (6-OH DA) into the unilateral substantia nigra. The contents of Met-enkephalin (MEK) and Leuenkephalin (LEK) in the CSF of the fourth ventricles of the normal control rabbits and those with destructive lesions in the substantia nigra were determined with radio-immunoassay. The concentrations of MEK and LEK in CSF of the rabbit models increased markedly to 14.3 and 28.2 folds in the controls respectively. The increased enkephalin content in CSF could be reduced to the normal level by intravenous administration of MIF-I. The results indicated that the action of MIF-I may be one of the important factors in alleviating the symptoms of parkinsonian patients.

Animals↗
PubMed1984

Uncomplicated selenium deficiency produced in chicks fed a corn-soy-based diet.

Day-old chicks were fed a practical-type diet based on corn- and soybean meal produced in a severely Se-deficient area of northeastern China. The diet contained 0.007 ppm Se and resulted in marked decreases in the activities of Se-dependent glutathione peroxidase in plasma and pancreas within 6 days of feeding. Chicks fed this basal diet showed histological signs of acinar atrophy of the pancreas, hyaline body formation, vacuolation and cytoplasmic shrinkage by 18 days and significantly elevated activities of amylase in plasma by 30 days. Each of these changes was prevented by supplementing the basal diet with Se to bring it to a level of 0.20 ppm. Chicks fed a Se-deficient purified diet based on crystalline amino acids also showed decreased Se-dependent glutathione peroxidase activities in plasma and pancreas, pancreatic damage as evidenced by histological examination and increases in plasma amylase activities. However, these signs of nutritionally induced pancreatic atrophy occurred sooner and were of greater magnitude than those observed in Se-deficient chicks fed the practical diet within the 30-day experimental period. These results, therefore, constitute the first report of nutritionally induced pancreatic atrophy in Se-deficient chicks fed a diet containing intact protein, and we suggest that a factor(s) associated with the practical diet acts to partially protect the chicks from this pathological consequence of severe Se deficiency.

Amylases↗