PubMed Health⌕ Search

Biomedical subjects

Z Jian

Publications and source records attributed to Z Jian.

31 records · Page 2Linked to original sources
PubMed1997

[Expression level of MDR1, and MRP in patients with malignant blood disease and its clinical significance].

RT-PCR method was used to detect the expression level of multi-drug resistance gene (MDR1) and multi-drug resistance associated protein (MRP) in patients with malignant blood disease, including 19 cases of acute leukemia and 6 cases of multiple myeloma. The results showed: expression level of MDR1 in patients with known clinical drug resistance elevated obviously and was significantly associated with clinical drug resistance (r = 0.612, P < 0.01), which indicated that expression of MDR1 was the main mechanism of clinical drug resistance. There is no obvious relationship between expression level of MDR1 and MRP (r = 0.035, P > 0.05).

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1997

[Relationship between urinary albumin excretion and blood vessel lesion in non-insulin-dependent diabetics].

To search the relationships between urinary albumin excretion and blood vessel lesion in non-insulin-dependent diabetics, we compared the differences of blood-lipid, blood pressure, coronary heart disease and retina disease between 58 patients. The group with microalbuminuria had significantly lower concentration of apolipoprotein A, and apolipoprotein A1/apolipoprotein B100 than that of the group with normal albuminuria, but there was no significant change in concentrations of trigly cerides, total cholesterol, high density lipoprotein, and apolipoprotein B100. Coronary heart disease and retina disease were significantly increased in group with microalbuminuria. There was negative correlation with apolipoprotein A1 and value of apolipoprotein A1/apolipoprotein B100, but positive correlation with systolic blood pressure by linear regression analysis for urinary albumin excretion.

Aged↗
PubMed1996

Nitric oxide production and expression of inducible nitric oxide synthase by bovine alveolar macrophages.

Alveolar macrophages play a central role in host defense in the lower respiratory tract. Production of the reactive intermediate nitric oxide (NO), via expression of inducible nitric oxide synthase (iNOS) is an important microbicidal effector mechanism possessed by macrophages. In this study, cytokine regulation of NO production by bovine alveolar macrophages (bAM) was evaluated. Bovine alveolar macrophages were exposed to one or more of the following: recombinant human (rh) and recombinant bovine (rb) IFN gamma, rh- and rbIL-1 beta, rbGM-CSF, rhTNF alpha, rhIL-4, endotoxin (LPS), fetal bovine serum (FBS), mitogen-stimulated bovine splenic supernatant (SS), and purified human TGF beta-1. LPS alone, or in combination with SS, rbIFN gamma, or rbIL-1 beta stimulated production of NO in a time and dose dependent fashion. Recombinant bovine IFN gamma, rbIL-1 beta, and rhTNF alpha in combination produced maximal stimulation which was not further enhanced by LPS. Recombinant human IFN gamma, rhIL-1 beta, and rbGM-CSF had minimal effect either as single stimuli, or in combination with LPS, rbIFN gamma, rbIL-1 beta, or rhTNF alpha. Nitric oxide production was inhibited by rhIL-4, and the L-arginine analogue antagonists of iNOS, N-G-monomethyl-L-arginine (NGMMA) and aminoguanidine (AG). Purified human TGF beta-1 did not inhibit NO production. Messenger RNA for iNOS was maximally expressed by 8 h and remained detectable for at least 48 h. Expression of iNOS mRNA induced by cytokines and LPS varied with strength of the stimulus as determined by nitrite production in culture supernatant.

Animals↗
PubMed1996

Activation of Ras and protection from apoptotic cell death by BDNF in PC12 cells expressing TrkB.

A clonal deoxyribonucleic acid (cDNA) clone of mouse trkB was expressed in cells of the rat PC12 pheochromocytoma cell line. The transformants followed apoptotic death upon serum deprivation. The addition of brain-derived neurotrophic factor (BDNF) to the culture medium supported the survival and neurite extension of the transformants in a serum-free condition. A Trk-family-specific protein kinase inhibitor, K-252a, inhibited the survival and neurite extension of the transformants in the presence of BDNF. BDNF activated autophosphorylation of trkB and caused the accumulation of a guanosine triphosphate (GTP)-bound form of Ras, both of which effects were also inhibited by K-252a. These results suggested that BDNF-triggered Ras activation is important for the survival and neuronal differentiation of PC12 cells in a serum-free condition.

Animals↗
PubMed1995

A study on oliguric standard in the elderly.

Water deprivation test was done in 44 healthy elderly persons, 26 were male, and 18 were female. They were deprived of the intake of water for 25 hours. The results showed that the maximal renal concentration function both in the elderly males and females was 887 +/- 91 mmol/L and 888 +/- 127 mmol/L respectively. The renal excretion of waste products in 24 hours both in the elderly males and females was 815 + 170 mmol/d and 620 + 132 mmol/d respectively. On the basis of point estimation, the minimal essential urine volume per day in the elderly males and females was 926 ml/d and 708 ml/d respectively, if the daily urine volume of the elderly is less than this level, then, the metabolic products generated per day can not be excreted by the kidney, and it would result in disorders of internal environment. Therefore, the oliguric standard in elderly males and females must be less than 926 ml/d and 708 ml per day respectively.

Age Factors↗
PubMed1993

Neural grafting to ischemic CA1 lesions in the rat hippocampus: an autoradiographic study.

Fetal hippocampal neurons were stereotaxically transplanted to five-day-old ischemic CA1 lesions in adult rat hippocampi. The recipient brains were examined 14 or 100 days later. The grafts survived well, and transplanted cells usually formed clusters in the host CA1 subfield. In vitro receptor autoradiography was employed to map the following receptors, the ligands indicated in parentheses being used for labeling: muscarinic cholinergic ([3H]quinuclidinyl benzilate), adenosine A1 ([3H]cyclohexyladenosine), kainate ([3H]kainic acid), spirodecanone ([3H]spiperone), opioid ([3H]naloxone), and GABAA ([3H]muscimol). The receptor autoradiographic technique showed significant binding of the six ligands in all hippocampal grafts two weeks after transplantation. One hundred days following transplantation, almost all receptors, especially muscarinic cholinergic, adenosine A1 and opioid receptor bindings in grafts, had significantly increased compared to bindings two weeks after transplantation. At this time, kainate and muscarinic cholinergic receptors in grafts had increased up to the near normal level of the CA1 in the hippocampus. Interestingly, adenosine A1 receptors in the grafted side had significantly increased not only in the CA1 but also in the stratum oriens of the CA3 compared with that in the non-grafted side. The increase of [3H]quinuclidinyl benzilate binding corresponded well with the innervation of acetylcholinesterase-positive fibers at 100 days after grafting. These results demonstrate that the transplanted neurons, which showed both pre- and post-synaptic autoradiographic markers in the ischemic CA1 lesions, are able to develop their properties and express the nature of normal hippocampal neurons.

Acetylcholinesterase↗
PubMed1992

The role of GTP binding proteins in ischemic brain damage: autoradiographic and histopathological study.

Cerebral ischemia produces perturbation of signal transduction systems in neurons. In order to estimate the contribution of guanine nucleotide-binding protein (G-protein) to hippocampal neuronal death, the effect of pertussis toxin (PTX) on the CA1 pyramidal cell damage after transient forebrain ischemia in rats was examined. PTX was administered 3 days before 20 min of transient forebrain ischemia. PTX injection into the CA1 subfield failed to alter the number of ischemic-damaged CA1 pyramidal cells. In contrast, ventricular PTX injection exacerbated CA1 pyramidal cell damage. We also studied postischemic alteration of GTP binding sites in the hippocampal formation using quantitative in vitro autoradiography. Autoradiographic imaging demonstrated predominant distribution of GTP binding sites in synaptic areas in the hippocampus. No significant change of GTP binding activity was observed in the hippocampus until 2 days after recirculation. Seven days after ischemia, when the CA1 pyramidal cells were depleted, the GTP binding sites of the strata oriens and radiatum in the CA1 subfield had reduced by 32% and 31%, respectively. In contrast, GTP binding in the CA3 subfield and the dentate gyrus remained unaltered throughout the reperfusion period. These results suggest that the amount of G-proteins as estimated by GTP binding remained unaltered in the hippocampus during the early recirculation period, when the CA1 pyramidal cells were morphologically intact, and that signal transduction pathways mediated by Gi and Go do not play a major role in delayed death of the CA1 pyramidal cells.

Animals↗
PubMed1991

Experimental pneumonia in mice produced by combined administration of Bordetella parapertussis and Pasteurella haemolytica isolated from sheep.

One-hundred-and-thirty-seven, 3-week-old, Swiss mice were inoculated intranasally with Bordetella parapertussis and Pasteurella haemolytica which had been isolated from naturally occurring cases of chronic non-progressive pneumonia in sheep. The combined administration produced a significantly more severe bronchopneumonia which occurred earlier, persisted for a longer period and involved a higher percentage of mice than that which was produced with B. parapertussis or P. haemolytica alone. These findings demonstrate an additive or synergic action between the two agents or their metabolic products, and provide indirect evidence that such interaction may occur in ovine chronic non-progressive pneumonia.

Animals↗
PubMed1990

Lafora's disease in an epileptic Basset hound.

A 6-year-old Basset hound developed a progressive central nervous system disease culminating in epileptic seizures. Histologically, Lafora bodies were found in neurones of the middle and deeper cerebral cortex and midbrain, in Purkinje cells and their processes, and in glial cells of the molecular layer of the cerebellum. Many were also observed free in the neuropil. The ultrastructural and histochemical characteristics of the bodies were similar to those described in previous human and canine cases of Lafora's disease.

Journal Article↗
PubMedDate not supplied

A novel bursting mechanism of type a neurons in injured dorsal root ganglia.

Using intracellular recording in vivo, the bursting behaviors were investigated in the neurons of chronically compressed dorsal root ganglia of the adult rat. In most cases, the first spike of a burst emerged from amplitude-increasing damped subthreshold membrane potential oscillation (SMPO) and the discharge terminated by an amplitude-decreasing damped SMPO. The rhythms of these bursting behaviors are all irregular. Since some researchers found that the stochastic dynamics can also produce similar bursting pattern, the deterministic dynamics of interevent interval (IEI) series obtained from raw membrane potential recording was detected by extraction of the hierarchy of unstable periodic orbits (UPOs) in the windowed IEI series. The results showed a number of statistically significant UPOs of order-one, order-two, and order-three. These orbits form a complex but predictable lattice of regions in which the dynamics of the bursting occurrence is deterministic. Based on a complete classification scheme, the investigated bursting can be depicted by the elliptic bursting dynamics. The significance of the finding that a neuron in the injured dorsal root ganglion has such dynamics is also discussed.

Action Potentials↗