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Biomedical subjects

C Tang

Publications and source records attributed to C Tang.

At least 163 records · Page 9Linked to original sources

Enforced expression of Bcl-XS induces differentiation and sensitizes chronic myelogenous leukemia-blast crisis K562 cells to 1-beta-D-arabinofuranosylcytosine-mediated differentiation and apoptosis.

Human chronic myelogenous leukemia-blast crisis K562 cells have been demonstrated to be relatively resistant to antileukemic drug-induced apoptosis. This has been attributed to the activity of p210bcr-abl tyrosine kinase present in the K562 cells, which is known to suppress drug-induced apoptosis. Recently, K562 cells have been shown to express the antiapoptosis Bcl-xL but not Bcl-2 proteins. To investigate the contribution of Bcl-xL toward resistance to drug-induced apoptosis, we created K562/Bcl-xS and K562/neo cells by electroporating the expression plasmids pSFFVneo-Bcl-xS and pSFFVneo, containing the bcl-xS and neomycin resistance genes, respectively, into K562 cells. K562/Bcl-xS but not K562/neo cells expressed the bcl-xS mRNA and p19Bcl-xS protein. In contrast, both cell types expressed equivalent levels of Bcl-xL, Bax, Bcl-2, Myc, retinoblastoma, p21cbor-abl, and p145abl proteins. A significant increase in the hemoglobin levels was observed in the K562/Bcl-xS compared with the K562/neo cells (P < 0.05). In addition, K562/Bcl-xS cells were significantly more sensitive than K562/neo cells to undergoing erythroid differentiation induced by low-dose 1-beta-D-arabinofuranosylcytosine (ara-C) and hexamethyl bisacetamide (P < 0.05), but not by all-trans-retinoic acid. Low-dose ara-C- or hexamethyl bisacetamide-induced differentiation was not associated with apoptosis of K562/Bcl-xS or K562/neo cells. Low-dose ara-C-induced erythroid differentiation was accompanied by conversion of the retinoblastoma protein to predominantly its underphosphorylated isoform as well as by down-regulation of Myc levels in K562/Bcl-xS and K562/neo cells. Importantly, exposure to high-dose ara-C (HIDAC; 100 microM ara-C for 4 h) caused internucleosomal DNA fragmentation and the morphological features of apoptosis in K562/Bcl-xS cells. These effects were modestly enhanced by cotreatment with HIDAC plus herbimycin A. In contrast, K562/neo cells were completely resistant to HIDAC- and herbimycin A-induced apoptosis. These results indicate that the expression of Bcl-xS induces erythroid differentiation and partially sensitizes chronic myelogenous leukemia-blast crisis-derived K562 cells to ara-C-induced differentiation and apoptosis.

Antimetabolites, Antineoplastic↗

[Protective effect of ATP-MgCl2 on gut mucosa in burn rat].

In order to study the protective effect of ATP-MgCl2 on gut mucosal barrier function in trauma-induced stressed animal, full thickness burn of 30% total body surface area (TBSA) was produced in rats, and ATP-MgCl2 was injected intraperitoneally right after scald-injury. Malondialdehyde (MDA) contents of ileum mucosa were determined and morphological alteration in the ileum was observed under light microscope. The results showed that ileum mucosal MDA content increased significantly, accompanied by obvious morphological change, after the injury, whereas MDA content was maintained at the normal control level and pathological alteration in ileum tissue was abated after the use of ATP-MgCl2. It suggests that ATP-MgCl2 possesses a protective effect on gut mucosal barrier function of scald-injured rat, and the mechanism involved may be related to the inhibition of lipid peroxidation in gut mucosa.

Adenosine Triphosphate↗

[Activation of CD4+ T cells and increased release of interleukin-5 in cultures of bronchoalveolar lavage cells and PBMC from patients with asthma].

To investigate the roles of CD4+ T cells and Th2 cytokine interleukin (IL)-5 in asthma, we examined the activation of CD4+ T cells and IL-5 production in cultures of bronchoalveolar lavage (BAL) cells and PBMC with and without allergen stimulation, in vitro, in 12 atopic asthmatic, 10 non-atopic asthmatic and 9 atopic non-asthmatic patients, as well as 10 normal control subjects. The patients with atopic and non-atopic asthma had significantly increased percentages of CD4+ T cells expressing CD25 (10.1% +/- 1.8% and 10.6% +/- 2.9%) and HLA-DR (11.2% +/- 3.1% and 12.0% +/- 3.6%, respectively) as compared with normal control subjects (P < 0.01) in unstimulated BAL cell cultures. IL-5 levels in the supernatants of those BAL cells from atopic and non-atopic asthmatic patients significantly enhanced (43.8 +/- 14.2 pg/ml and 85.5 +/- 15.1 pg/ml) as compared with those for atopic non-asthmatic and normal control subjects (P < 0.01). Meanwhile, increased percentages of activated CD4+ T cells and IL-5 secretion were also observed in the cultures of unstimulated PBMC from both types of asthmatic patients. In the cultures of allergen-stimulated BAL cells and PBMC, atopic asthmatic patients demonstrated marked increase in the percentage of CD4+ CD25+ T cells (17.9% +/- 13.9% and 29.0% +/- 27.5%) and IL-5 production (30.5 +/- 13.3 pg/ml and 109.3 +/- 35.0 pg/ml, for BAL cell and PBMC cultures respectively) as compared with nona-topic asthmatic patients (P < 0.01). Although the percentages of activated CD4+ T cells and IL-5 secretion elevated significantly in allergen-stimulated culture of PBMC from atopic non-asthmatic subjects, the IL-5 release by the allergen-stimulated BAL cells from the same subjects were still significantly lower than both forms of asthmatic patients (P < 0.01). Our findings show that activation of CD4+ T cells and IL-5 production are strongly implicated in the pathogenesis of both atopic and non-atopic asthma.

Adult↗

[Experimental research of the influences on the development of the hip joints with excavated acetabula].

There are still arguments about the operation excavated acetabula treatments for the congenital dislocation of the hip. To inquire into the influences on the development of the hip joints with excavated acetabula size, we divided 60 two-month-old chickens into three groups which were given incised dislocation and then reduction partly excavated the cartilages of the acetabula and excavated them totally to the left hips respectively. Contrasting observation of all the experimental chickens was taken on the right ones of their own. The second group achieved a fair function of the joint movement. Limited and slight adhesion was not affecting the development of the joints seriously. The third group had, on the contrary, poor functions because of the comprehensive adhesion in the acetabula. The surfaces of the acetabula were replaced by fabric tissue. The remaining or regenerating cartilage cells vary obviously under the light scope and the electronic scope. The heads of the femurs had changed similarly. It is suggested that in dealing with the congenital dislocation of the hip, excavating the acetabola cartilage is not advisable. Partly excavating is permitted when a limited bony process existing in the bottom of the acetabula.

Acetabulum↗

[Reasonability of extracting procedures for huiyangfanben decoction].

The reasonability of extracting procedures for traditional Chinese prescriptions was studied with Huiyangfanben Decoction as sample. The comparative results of the ingredients in extractions prepared by different procedures revealed. For the prescriptions with complicated ingredients, more attention should be paid to the ingredients and their characteristics when designing the extracting procedurs, and in extraction the drugs should be classified according to the interaction of the ingredients. More extracting solvents could be used according to the characteristics of the active ingredients.

Aconitine↗

A natural disruption of the secretory group II phospholipase A2 gene in inbred mouse strains.

The synovial fluid or group II secretory phospholipase A2 (sPLA2) has been implicated as an important agent involved in a number of inflammatory processes. In an attempt to determine the role of sPLA2 in inflammation, we set out to generate sPLA2-deficient mice. During this investigation, we observed that in a number of inbred mouse strains, the sPLA2 gene was already disrupted by a frameshift mutation in exon 3. This mutation, a T insertion at position 166 from the ATG of the cDNA, terminates out of frame in exon 4, resulting in the disruption of the calcium binding domain in exon 3 and loss of both activity domains coded by exons 4 and 5. The mouse strains C57BL/6, 129/Sv, and B10.RIII were found to be homozygous for the defective sPLA2 gene, whereas outbred CD-1:SW mice had variable genotype at this locus. BALB/c, C3H/HE, DBA/1, DBA/2, NZB/BIN, and MRL lpr/lpr mice had a normal sPLA2 genotype. The sPLA2 mRNA was expressed at very high levels in the BALB/c mouse small intestine, whereas in the small intestine of the sPLA2 mutant mouse strains, sPLA2 mRNA was undetectable. In addition, PLA2 activity in acid extracts of the small intestine were approximately 40 times higher in BALB/c than in the mutant mice. Transcription of the mutant sPLA2 gene resulted in multiple transcripts due to exon skipping. None of the resulting mutant mRNAs encoded an active product. The identification of this mutation should not only help define the physiological role of sPLA2 but also has important implications in mouse inflammatory models developed by targeted mutagenesis.

Amino Acid Sequence↗

A positron emission tomography [18F]deoxyglucose study of developmental stuttering.

Positron emission tomography using [18F]deoxyglucose (FDG) as a marker of regional brain metabolism was used to investigate the neural substrate of stuttering. Four patients with severe developmental stuttering were studied while reading aloud to another person (stuttering condition) and while reading aloud in unison with someone else (non-stuttering condition). The patients were also compared with four normal controls reading aloud by themselves. In the stuttering condition, significant decreases in regional glucose metabolism in Broca's area, Wernicke's area and frontal pole were seen compared with themselves while not stuttering. These differences were also seen in stuttering condition compared with normal controls. Significantly lower left caudate metabolism was seen in patients during both stuttering and non-stuttering conditions compared with normal controls. A circuit for stuttering is proposed based on these findings.

Adult↗

Multi-shot EPI for improvement of myocardial tag contrast: comparison with segmented SPGR.

To assess the potential value of multi-shot EPI relative to segmented k-space SPGR for myocardial tagging, we measured tag contrast for both sequences in a phantom and human study and compared it with theoretical predictions. In the human heart, EPI tag contrast was three times that of SPGR at the end of systole. Tag duration was lengthened with EPI to at least 600 ms. In addition, the entire heart was examined in a total of 32 heartbeats with EPI versus 152 heartbeats with SPGR.

Algorithms↗

Responsiveness to stem cell factor (SCF) of peripheral blood colony-forming cells from patients with myelodysplastic syndromes (MDS).

We have previously reported that serum stem factor (SCF) levels are significantly lower in patients with myelodysplastic syndrome (MDS) than normal controls. We have now studied the effects of adding SCF to cultures of blood mononuclear cells from patients with MDS and normal subjects. Three of 17 patients with MDS showed marked increases in erythroid colony numbers with SCF + erythropoietin compared to interleukin-3 + erythropoietin. In two cases (1RA and 1ISA) the erythroid colony numbers became normal. The same RA patient also showed a marked increase in myeloid colony numbers, which were undetectable with granulocyte-macrophage colony-stimulating factor alone, but within the normal range when SCF was added. A fourth patient (ISA) showed a 4.7-fold increase in myeloid colonies with SCF, but no erythroid response. The normal subjects showed a trend towards increased numbers of myeloid colonies with SCF; erythroid colonies did not increase. A correlation was found between the MDS patients' haemoglobin levels and erythroid colony numbers with and without SCF, but there was no correlation between erythroid or myeloid colonies in the presence of SCF and their serum SCF level.

Adult↗

Regulation of the ferredoxin component of renal hydroxylases at transcriptional and postranslational levels and of the protein inhibitor of cyclic AMP-dependent kinase.

We have studied two proteins potentially involved in the regulation of the 25-OH-D-1-hydroxylase, which is located in the renal mitochondria and which is responsible for the production of the steroid hormone 1,25(OH)2D3. The endogenous inhibitor of cyclic AMP-dependent protein kinase, PKI, is down regulated by 1,25(OH)2D3. Having cloned and sequenced PKI cDNA, we studied its message levels and found them to be regulated by 1,25(OH)2D3 tissue specifically in the kidney and in kidney cell culture. In other experiments we over expressed the ferredoxin component of the 1-hydroxylase and found it to be physically and chemically indistinguishable from those of classic steroidogenic tissues. The mRNA encoding the ferredoxin component is up-regulated by chronic vitamin D deficiency, which at the same time leads to sustained elevation in 1-hydroxylase activity; no short term effect of 1,25(OH)2D3 on ferredoxin mRNA in kidney cell culture could be demonstrated. Finally, there was an association between decreased phosphorylation of ferredoxin and decreased 1-hydroxylase activity brought about by treatment of cultured kidney cells with TPA. Control of the renal signaling events involved in the production of 1,25(OH)2D3 remains a fruitful area of investigation in the field of the metabolism and actions of vitamin D and its metabolites.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

Gut peptide receptors in pancreata of azaserine-treated and normal control rats.

Gut peptides are involved in the growth and carcinogenesis of the exocrine pancreas of rats after treatment with azaserine. However, little is known about the influence of azaserine on expression of gut peptide receptors in the pancreas of the rat. Cholecystokinin, bombesin, somatostatin, secretin, and vasoactive intestinal peptide receptors were therefore visualized and quantified by storage phosphor autoradiography in pancreata of either saline control or azaserine-treated rats. As expected, putative preneoplastic lesions were formed in the pancreata of the azaserine-treated but not in the control animals. The pancreata of control rats contained receptors for cholecystokinin, bombesin, somatostatin, secretin, and vasoactive intestinal peptide. Cholecystokinin receptors were of the A-type and showed, in contrast to the other receptors, a heterogeneous expression due to variability of the high-affinity receptors. In the pancreata of azaserine-treated animals a significantly increased binding capacity of high-affinity receptors fro cholecystokinin was found not only in atypical acinar cell nodules but also in non-nodular pancreas when compared to pancreas of control rats (P < 0.05). Neither atypical acinar cell nodules nor non-nodular pancreas of rats treated by azaserine were shown to possess receptors for the other four types of gut peptide receptors. The spectrum of peptide receptors in pancreas of control and azaserine-treated rats in this study may help to understand the mechanism whereby gut hormones may modulate pancreatic carcinogenesis.

Animals↗

pIXY321 protects against Ara-C or taxol-induced apoptosis and loss of clonogenic survival of normal human bone marrow progenitor cells.

By suppressing apoptosis, hemopoietic growth factors (HGFs) promote the survival of CD34+, HLA-DR+ marrow cells that are enriched for hemopoietic progenitor cells (HPC). In the present studies, we have examined the effects of pIXY321, a genetically engineered fusion protein of GM-CSF and IL-3 (GM-CSF/IL-3), on high-dose Ara-C (HIDAC) and taxol-induced apoptosis and survival of a multilineage HPC, the CFU-GEMM. Exposure to 1.0 mumol/l taxol for 24 h or HIDAC > or = 10 mumol/l for 4 h induced internucleosomal DNA fragmentation and the morphologic features of apoptosis in CD34+, HLA-DR+ cells. These treatments were associated with > or = 50% inhibition of the assayable CFU-GEMM colony numbers. Incubation in serum-free medium (SFM) alone for 24 h also induced apoptosis of CD34+, HLA-DR+ cells, which was associated with reduced intracellular levels of the bcl-2 gene product p26BCL-2. Co-treatment with pIXY321 (10 ng/ml) inhibited apoptosis of CD34+, HLA-DR+ cells incubated in SFM, without significantly increasing the intracellular p26BCL-2 levels. Furthermore, co-treatment with pIXY321 significantly reduced taxol- and Ara-C-induced apoptosis and promoted the survival of CFU-GEMM (P < 0.05). Taxol and Ara-C mediated apoptosis of CD34+, HLA-DR+ cells, and its inhibition by pIXY321, was not accompanied by any significant alteration in the intracellular p26BCL-2 levels. By demonstrating that co-treatment with pIXY321 confers significant protection against apoptosis of CD34+, HLA-DR+ cells as well as promotes survival of normal HPC exposed to clinically relevant schedules and concentrations of taxol of Ara-C, these results support the design of chemotherapy regimens incorporating pIXY321 plus taxol and/or high-dose Ara-C for solid tumors and/or acute leukemias. It is hoped that the use of such a cytokine might maintain normal HPC numbers following chemotherapy, therefore avoiding prolonged suppression.

Antigens, CD34↗

[Some biochemical indexes in white rabbit's blood affected by acute high intensity microwave].

Irradiation of white rabbits by 10, 50, 100 and 200 mW/cm2 microwave respectively can cause the disorder of protein metabolism, the abnormality of blood sugar, and the change of the activity of serum alpha-hydroxybutyrate dehydrogenase, lactate dehydrogenase, glutamic oxalacetic transaminase, glutamic pyruvic transaminase, acid phosphatase ect. These changes can be used as indexes in the evaluation of the effect of acute high intensity microwave exposure. The effect on the organism mainly depends on the intensity of exposure provided the dose of microwave remains the same.

Acid Phosphatase↗

Localization and quantification of cholecystokinin receptors in rat brain with storage phosphor autoradiography.

The present study evaluated a new imaging technique that demonstrated the application of storage phosphor autoradiography in the localization and quantification of cholecystokinin receptors in rat brains and compared the results with film autoradiography. Cryostat sections were incubated with [125I]Bolton-Hunter-labeled sulfated cholecystokinin octapeptide followed by exposure to a storage phosphor-imaging screen and suitable autoradiography film. To obtain satisfactory images, it took 6 days with film autoradiography vs. 15 hours with the storage phosphor technique. Both film and storage phosphor autoradiograms showed the same cholecystokinin receptor distribution in brain sections; however, the film imaged more details. To reach the lowest possible response ratio between low and high receptor density regions in rat brains, storage phosphor autoradiography was about 240-fold faster than film. In addition, the new technique presented a considerably larger exposure time range for maintaining that ratio. The binding per area showed a linear relationship with the thickness of sections between 5 and 14 microns. In the linear response range, the quantitative results of both methods are comparable. In conclusion, storage phosphor autoradiography is a faster technique for localizing and quantifying peptide receptors in tissue sections but slightly compromised in resolution when compared with film autoradiography.

Animals↗