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Biomedical subjects

J Tian

Publications and source records attributed to J Tian.

At least 145 records · Page 8Linked to original sources
PubMed1996

Brain substrates activated by electroacupuncture of different frequencies (I): Comparative study on the expression of oncogene c-fos and genes coding for three opioid peptides.

Low and high frequency electroacupuncture (EA)-produced analgesia have been shown to be mediated by different brain substrates and different opioid peptides. In this study, Fos-like immunoreactivity (FLI) and in situ hybridization of the three opioid mRNAs were used to examine the effect of low (2 Hz) and high (100 Hz) frequency EA on neuronal activities, and the expression of opioid genes. 2 Hz and 100 Hz EA induced a markedly different spatial patterns of Fos expression in the rat brain, suggesting there are distinct neuronal pathways underlying EA of different frequencies. Likewise, 2 Hz and 100 Hz EA exert differential effects on opioid gene expression: while 2 Hz EA induced a more extensive and intensive preproenkephalin (PPE) mRNA expression than 100 Hz EA, it had no effect on preprodynorphin (PPD) mRNA expression which was significantly increased by 100 Hz EA stimulation. In contrast, EA of both frequencies did not affect POMC mRNA expression.

Animals↗
PubMed1996

Brain substrates activated by electroacupuncture (EA) of different frequencies (II): Role of Fos/Jun proteins in EA-induced transcription of preproenkephalin and preprodynorphin genes.

Antisense oligodeoxynucleotides (ODNs) of c-fos and/or c-jun were used in this study to investigate the role of Fos and Jun proteins in electroacupuncture (EA)-induced transcription of the opioid genes, preproenkephalin (PPE), preprodynorphin (PPD) and proopiomelanocortin (POMC). As the results showed, EA-induced Fos and fun expression was blocked efficiently and specifically by e-fos and c-jun antisense ODNs, respectively. This treatment significantly prevented EA-induced PPD, but not PPE, mRNA expression. These results suggest that Fos and Jun proteins are involved in PPD rather than PPE gene transcription activated by EA stimulation.

Animals↗
PubMed1996

Functional site in alpha-lactalbumin encompasses a region corresponding to a subsite in lysozyme and parts of two adjacent flexible substructures.

Aromatic cluster 1 of alpha-lactalbumin (LA), a substructure adjacent to the cleft, is important for its interaction with galactosyltransferase (GT) and effects on glucose binding in the lactose synthase complex [Grobler, J. A., Wang, M., Pike, A. K., & Brew, K. (1994) J. Biol. Chem. 269, 5106-5114]. The full extent of the functional region in LA has been probed by mutagenesis of residues that are near aromatic cluster 1 or within the cleft that corresponds to the active site in the homologous type c lysozymes. The conserved residues Val42, Gln54, and Ile59, which correspond to residues of lysozyme that act in substrate binding in subsites C to E, together with residues adjacent to aromatic cluster 1, were found to be not required for activity. In contrast, replacing Leu110, a component of the region corresponding to lysozyme subsite F, with His or Glu greatly reduces the affinity of LA for GT while the introduction of Arg lowers the synergism of LA and glucose binding to GT and also reduces the affinity of LA for GT. Substitutions for Ala106, which is adjacent to Leu110 in the structure, also perturb activity. The region of the cleft corresponding to subsite F is important for function in LA as well as in lysozyme since other components of this subsite, His32 and Phe31, are also crucial for LA activity. The qualitatively different effects of various substitutions for Leu110 may be mediated by their influence on His32 or by changes in the structure of the lactose synthase complex.

Amino Acid Sequence↗
PubMed1996

C-Fos proteins are not involved in the activation of preproenkephalin gene expression in rat brain by peripheral electric stimulation (electroacupuncture).

The present work was designed to study the role of the oncogene product c-Fos in activating the transcription of preproenkephalin (PPE) gene following a kind of peripheral electric stimulation known as electroacupuncture (EA) stimulation. The temporal patterns of rat brain c-fos and PPE mRNA expression were evaluated using the method of Northern blotting, showing that c-fos mRNA expression, which peaked at 2 h after the termination of EA, was always ahead of the PPE mRNA expression which began at 4 h and peaked at 48 h after EA. The methods of immunocytochemistry (ICC) and in situ hybridization (ISH) techniques were combined to identify the co-existence of c-Fos protein and PPE mRNA at the cellular level. The results showed that only a small percentage of PPE mRNA-containing neurons depicts Fos-like immunoreactive nuclei. These findings suggest that c-Fos protein may not be involved in the activation of brain PPE gene transcription induced by peripheral electric stimulation.

Animals↗
PubMed1996

Nasal administration of glutamate decarboxylase (GAD65) peptides induces Th2 responses and prevents murine insulin-dependent diabetes.

We previously demonstrated that a spontaneous Th1 response against glutamate decarboxylase (GAD65) arises in NOD mice at four weeks in age and subsequently T cell autoimmunity spreads both intramolecularly and intermolecularly. Induction of passive tolerance to GAD65, through inactivation of reactive T cells before the onset of autoimmunity, prevented determinant spreading and the development of insulin-dependent diabetes mellitus (IDDM). Here, we examined whether an alternative strategy, designed to induce active tolerance via the engagement of Th2 immune responses to GAD65, before the spontaneous onset of autoimmunity, could inhibit the cascade of Th1 responses that lead to IDDM. We observed that a single intranasal administration of GAD65 peptides to 2-3-wk-old NOD mice induced high levels of IgG1 antibodies to GAD65. GAD65 peptide treated mice displayed greatly reduced IFN gamma responses and increased IL-5 responses to GAD65, confirming the diversion of the spontaneous GAD65 Th1 response toward a Th2 phenotype. Consistent with the induction of an active tolerance mechanism, splenic CD4+ (but not CD8+) T cells from GAD65 peptide-treated mice, inhibited the adoptive transfer of IDDM to NOD-scid/scid mice. This active mechanism not only inhibited the development of proliferative T cell responses to GAD65, it also limited the expansion of autoreactive T cell responses to other beta cell antigens (i.e., determinant spreading). Finally, GAD65 peptide treatment reduced insulitis and long-term IDDM incidence. Collectively, these data suggest that the nasal administration of GAD65 peptides induces a Th2 cell response that inhibits the spontaneous development of autoreactive Th1 responses and the progression of beta cell autoimmunity in NOD mice.

Administration, Intranasal↗
PubMed1996

Segmentation of auditory brainstem response signals.

Auditory brainstem responses are used to detect hearing defects in audiology and otoneurology. The use of computer programs for the analysis of such recordings is increasing. To identify their detailed properties a pattern recognition algorithm implemented in an analysis program must be highly reliable. For the recognition process, some preprocessing phases after recording the necessary, such as filtering and often also segmentation. In the following, we will explore segmentation, which can be used in preprocessing of biomedical signals after filtering. We studied linear segmentation, where slopes of short signal segments are computed and divided into different classes according to their values. A segment length of 8 samples for a sampling frequency of 50 kHz employed was best according to our tests and error criteria. Using clustering, we found that less than 10 segment classes is suitable for pattern recognition.

Algorithms↗
PubMed1996

Insulin and angiotensin II are additive in stimulating TGF-beta 1 and matrix mRNAs in mesangial cells.

Angiotensin II (Ang II) and insulin are implicated in the mesangial cell hypertrophy and excessive accumulation of mesangial matrix seen in glomerulosclerosis. Therefore, the effects of Ang II with and without insulin on mRNA levels of several important extracellular matrix genes and transforming growth factor beta-1 (TGF-beta 1) were examined. Ang II alone (1 microM) added to quiescent, murine mesangial cells in serum-free, insulin-free media slightly but not significantly increased TGF-beta 1, fibronectin, collagen I, collagen IV and laminin message levels. The slight elevations in message expression were reversed by losartan, suggesting that these modest effects are mediated by the AT-1 receptor. Ang II alone also had no significant effects on TGF-beta 1 and extracellular matrix message levels in quiescent rat mesangial cells. In contrast, significant increases in mRNA for collagen 1 (6-fold), collagen IV (4-fold), fibronectin 1 (4-fold) and TGF-beta 1 (2-fold) were seen with insulin alone (10(-6)M) in rat mesangial cells, and a dose-response effect could be demonstrated for insulin (10(-9) to 10(-6)M). Ang II plus insulin further significantly increased collagen I (9-fold), collagen IV (9-fold), fibronectin 1 (5-fold) and TGF-beta 1 (3-fold) message expression. These effects were partially reversed in the presence of losartan. The Northern analyses were supported by measurements of active and total TGF-beta 1 activity (pg/ml/ 5 x 10(6) cells): 1145 +/- 76 and 1960 +/- 199, serum free control; 1121 +/- 92 and 1932 +/- 214, Ang II (10(-6)M); 4589 +/- 103 (P < 0.001 vs. control) and 11071 +/- 1952 (P < 0.01 vs. control), insulin (10(-6)M); and 6881 +/- 183 (P < 0.001 vs. control) and 16626 +/- 1435 (P < 0.01 vs. control), insulin plus Ang II. These results suggest that insulin, itself, significantly increases TGF-beta 1 and extracellular matrix gene expression in rat mesangial cells. Ang II alone has modest effects, while Ang II and insulin have additive effects. To explain the mechanism of these additive effects, we investigated the action of Ang II on insulin signaling and the effect of insulin on Ang II AT1 receptor mRNA expression. Ang II did not enhance insulin-induced insulin receptor substrate-1 (IRS-1) phosporylation or phosphatidylinositol3 (PI-3) kinase activity, but did enhance insulin-induced mitogen activated protein (MAP) kinase activity. Insulin increased message levels of AT1 receptor by twofold. These results suggest that enhancement of MAP kinase activity and AT1 receptor regulation by insulin may contribute to the additive effects of insulin and Ang II in mesangial cells.

Angiotensin II↗
PubMed1996

Modulating autoimmune responses to GAD inhibits disease progression and prolongs islet graft survival in diabetes-prone mice.

In nonobese diabetic (NOD) mice, beta-cell reactive T-helper type 1 (Th1) responses develop spontaneously and gradually spread, creating a cascade of responses that ultimately destroys the beta-cells. The diversity of the autoreactive T-cell repertoire creates a major obstacle to the development of therapeutics. We show that even in the presence of established Th1 responses, it is possible to induce autoantigen-specific anti-inflammatory Th2 responses. Immune deviation of T-cell responses to the beta-cell autoantigen glutamate decarboxylase (GAD65), induced an active form of self-tolerance that was associated with an inhibition of disease progression in prediabetic mice and prolonged survival of syngeneic islet grafts in diabetic NOD mice. Thus, modulation of autoantigen-specific Th1/Th2 balances may provide a minimally invasive means of downregulating established pathogenic autoimmune responses.

Adoptive Transfer↗
PubMed1996

Constitutively active G(S) alpha-subunits stimulate Pit-1 promoter activity via a protein kinase A-mediated pathway acting through deoxyribonucleic acid binding sites both for Pit-1 and for adenosine 3',5'-monophosphate response element-binding protein.

Constitutively active mutations of the G protein alpha(S) subunit are detected at a high frequency in human pituitary adenomas that secrete GH or PRL. It seems possible that over-expression of the pituitary cell-specific transcription factor Pit-1/GHF-1 (Pit-1) gene in response to active alpha(S) subunits contributes to the formation of these adenomas. We have examined whether expression in pituitary cells of one of these constitutively active alpha(S) subunits, Q227L-alpha(S), stimulates expression directed by the Pit-1 promoter. Transient expression of Q227L-alpha(S) yielded a strong stimulation of a target Pit-1 promoter-chloramphenicol acetyl transferase (CAT) construct, (-200)Pit-1-CAT. Expression of wild-type alpha(S) or an inactive alpha(S) mutant yielded, respectively, reduced or no stimulation of CAT activity. A dominant inhibitor of protein kinase A (PKA), RAB, blocked almost completely either forskolin (FSK) or Q227L-alpha(S) stimulation of (-200)Pit-1-CAT expression, implying that PKA is required for the action of Q227L-alpha(S) on the Pit-1 promoter. The Pit-1 promoter contains a binding site for Pit-1 and two CREB binding sites. Mutation of the Pit-1 binding site reduced but did not eliminate either FSK or Q227L-alpha(S) stimulation of Pit-1 promoter activity, implying a partial but incomplete requirement for this element for a PKA-mediated response to Q227L-alpha(S). The CREB dominant inhibitor S133A-CREB yielded a partial reduction in either FSK or Q227L-alpha(S) stimulation of (-200)Pit-1-CAT expression, implying that one or both of the Pit-1 promoter adenosine 3'5'-monophosphate response element binding protein (CREB) binding sites is/are also required for a complete PKA-mediated response to Q227L-alpha(S). The observation that S133A-CREB completely blocked the response to FSK or Q227L-alpha(S) of a Pit-1 promoter containing a mutated site PitB1 implies that the binding sites for Pit-1 and CREB account for all of the response elements for FSK or alpha(S) in the Pit-1 promoter.

Animals↗
PubMed1996

[A study on risk factors of neural tube defects].

One hundred and twenty-three cases with neural tube defects collected during 1991 to 1993 from 12 hospitals with birth defect surveillance in Hebei Province, and their pair-matched controls were analyzed with single and multiple conditional logistic regression to study the effects of food and drinking water on occurrence of neural tube defects. Results showed factors contributing to neural tube defects were maternal previous history of birth defects, much consumption of dried and pickled vegetables during pregnancy, too much nitrate content in drinking water (containing more than 10 mg nitrogen per liter of water), less consumption of meat, eggs, and beans in their diet.

China↗
PubMed1996

Exercise echocardiography: feasibility and value for detection of coronary artery disease.

OBJECTIVE: To evaluate the feasibility and accuracy of exercise echocardiography (Ex-Echo) for the diagnosis of coronary artery disease (CAD) based on coronary angiography (CA). PATIENTS AND METHODS: Forty-seven patients were found to have CAD and examined by upright exercise electrocardiography (Ex-ECG) on a treadmill within two weeks of CA. Before and immediately after exercise, the patients lay on a bed beside the treadmill in the left lateral position and parasternal long and short axis and apical two and four chamber views of the heart were acquired. Pre- and post-echocardiograms were analysed in a side-by-side multiple screen format on the imaging view and hypodynamic wall motion of the left ventricle after exercise was defined as Ex-Echo positive. The sensitivity, specificity and predictive accuracy of Ex-Echo and Ex-ECG were calculated on the basis of CA data. RESULTS: Satisfactory echocardiograms were recorded in 46 patients after exercise. The success rate was 97.8%. Compared with Ex-ECG, Ex-Echo was more sensitive (87.5% vs 62.5%, P < 0.05), specific (92.8% vs 60.0%, P < 0.05) and accurate (89.4% vs 61.7%, P < 0.01). The concord of determining the number of diseased vessels between coronary angiography and Ex-Echo was 90.9% in single vessel disease and 45.0% in multiple vessel disease. Wall motion scoring index, however, was higher in multiple than in single vessel CAD. CONCLUSIONS: Ex-Echo test is feasible and accurate in detecting CAD and wall motion scoring index is probably useful in distinguishing multiple from single vessel CAD.

Coronary Disease↗
PubMed1996

[Constituents of essential oil of imported myrrh and gum opoponax].

The constitutents of essential oil in two kinds of Myrrha were analyzed by GC-MS. Fifteen compounds in Myrrh and thirty-three compounds in Gum opoponax were identified with their percent contents given. The main constituent of Myrrh is furanoeudesma-1,3-diene, and the main constituent of Gum opoponax is beta-trans-ocimene.

Drugs, Chinese Herbal↗
PubMed1996

[Factors affecting survival of hepatic carcinoma patients and their clinical significance].

UNLABELLED: 621 patients with unresectable hepatocellular carcinoma were given more than 2 times of intervention treatment. The correlations between the survival rates, tumor histology, portal tumor thrombus and the method and frequency of intervention treatment were analyzed. RESULTS: (1) The survival rates were higher in cases with single nodular tumor than in those with diffuse-tumors. (2) The survival rates of cases without tumor thrombus in portal system were significantly higher than those with tumor thrombus. However, no correlation was found between the survival rates and the location of thrombus in portal vein. (3) Intraarterial drug infusion combined with lipoidol plus gelatin sponge embolization gave the best therapeutic resalts. (4) How frequent was the intervention would be determined by the patients' general condition and was dependent on the quality of treatment. The cumulative survival rates were greatly affected by the above-mentioned factors. The treatment needs to be individualized.

Adult↗
PubMed1996

[Expression of retroviral transmembrane envelope protein p15E in human malignant cells].

Malignant tumor growth is always accompanied with immune suppression. Tumor-derived immuno-suppressive factors, among others, are thought to be responsible, but their nature is not well defined. The paper reports on the expression of an immuno-suppressive retroviral transmembrane envelope protein p15E at different levels in human cancer cells. By using immunohistochemistry, enzyme-linked immunosorbent assay, flow cytometry and in situ hybridization, p15E expression could be demonstrated in cancers of the esophagus, nosopharynx, rectum, ovary (including malignant effusion and cell lines), stomach and breast. Enhanced expression of p15E was also observed in activated lymphocytes of cancer patients as shown by RT-PCR technique. The results indicate that p15E of tumor origin, and perhaps that from activated lymphocytes, may contribute to the immune suppression associated with malignancy.

Gene Products, gag↗
PubMed1995

Decreased atherosclerosis in mice deficient in both macrophage colony-stimulating factor (op) and apolipoprotein E.

To develop a murine model system to test the role of monocyte-derived macrophage in atherosclerosis, the osteopetrotic (op) mutation in the macrophage colony-stimulating factor gene was bred onto the apolipoprotein E (apoE)-deficient background. The doubly mutant (op/apoE-deficient) mice fed a low-fat chow diet had significantly smaller proximal aortic lesions at an earlier stage of progression than their apoE-deficient control littermates. These lesions in the doubly mutant mice were composed of macrophage foam cells. The op/apoE-deficient mice also had decreased body weights, decreased blood monocyte differentials, and increased mean cholesterol levels of approximately 1300 mg/dl. Statistical analysis determined that atherosclerosis lesion area was significantly affected by the op genotype and gender. The confounding variables of body weight, plasma cholesterol, and monocyte differential, which were all affected by op genotype, had no significant additional effect on lesion area once they were adjusted for the effects of op genotype and gender. Unexpectedly, there was a significant inverse correlation between plasma cholesterol and lesion area, implying that each may be the result of a common effect of macrophage colony-stimulating factor levels. The data support the hypothesis that macrophage colony-stimulating factor and its effects on macrophage development and function play a key role in atherogenesis.

Animals↗
PubMed1995

Constitutively active Gq-alpha stimulates prolactin promoter activity via a pathway involving Raf activity.

We have investigated the ability of a constitutively active Gq-alpha mutant, Q209L-alpha q, to regulate target gene expression. Transient expression in GH3 pituitary cells of a rat proximal prolactin promoter-chloramphenicol acetyltransferase construct (-187)PRL-CAT, was stimulated by co-expression of Q209L alpha q, but not by wild-type alpha q. Q209L-alpha q stimulated expression of constructs driven by promoters for either rat prolactin or growth hormone, but not of a control construct driven by the thymidine kinase promoter. Thus, transcriptional effects of alpha q are specific both for the activated state of this G-alpha subunit and the promoter examined. Since both the prolactin and growth hormone promoters are activated by the pituitary cell-specific transcription factor Pit-1, we examined whether a Pit-1 binding site could direct a response to Q209L-alpha q. Two copies of prolactin promoter Pit-1 binding site 1P conferred upon a heterologous metallothionein promoter a response to Q209L-alpha q, implying an involvement of this site in the transcriptional action of Q209L-alpha q on the prolactin promoter. The phorbol ester activator of protein kinase C, 12-O-tetradecanoylphorbol-13-acetate, stimulated (-187)PRL-CAT activity, but opposed the action of Q209L-alpha q on activity of this PRL-CAT construct. Q209L-alpha q stimulation of (-187)PRL-CAT activity was inhibited by co-expression of a dominant negative Raf mutant, Raf-C4, but not by a point mutant of Raf-C4 with reduced inhibitory properties. These results imply that activated alpha q subunits can stimulate prolactin promoter activity via a pathway that involves a Pit-1 DNA binding site(s), is opposed by protein kinase C, and is mediated by a pathway in which Raf-1 kinase plays a role.

Animals↗