Combination chemotherapy with DATV regimen in treatment of adult acute nonlymphocytic leukemia.
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Biomedical subjects
Publications and source records attributed to Q Zhou.
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This study investigated the modifying effect of 26-hydroxycholesterol (26-OHC) on low-Mg(2+)-induced atherosclerotic changes in human arterial smooth muscle cells. Cells were exposed to a medium containing a concentration of 142, 332, 665 and 949 microM Mg2+ (as control) for the designed periods. Half the cells were simultaneously exposed to 10 micrograms/ml of 26-OHC. The results showed that the cytotoxicity of low Mg2+ and the stimulating effect of low Mg2+ on cytosolic free Ca2+ level and 45Ca2+ uptake were accentuated by 26 microns OHC. The significant increase of [3H]thymidine incorporation by Mg2+ level at and lower than 332 was, however, counteracted by 26-OHC. While an increased [3H]leucine incorporation occurred only at a level of 665 microM Mg2+, an additional increase of [3H]leucine incorporation also occurred at a level of 142 microM Mg2+ in the presence of 26-OHC. We suggest that 26-OHC could modify the atherogenic effect of low Mg2+.
No transformant was obtained when pIJ702 (tsr,mel+) from S. lividans TK24 was used to transform S. hygroscopicus 10-22. pIJ702 isolated from S. fradiae ATCC 10745, however, was transformed into 10-22 at a frequency of 10(3)-10(4) transformants/micrograms DNA. Among the transformant colonies, only 1/1000 of them were black in colour (mel+) while a great majority of them remained white (mel-). Plasraid pIJ702 band was only visualized on agarose gels from the black colonies but not from the white colonies. However, when pIJ702 isolated from both black and white transformants were used to transform S. lividans TK24, the mel gene was expressed normally in the recipients. The preparations was also successful in transforming S. hygroscopicus 10-22, and again gave rise to 1/1000 of black colonies only. When the 10-22 (pIJ702) black colonies were plated on non-selective medium, among the majority of black colonies grown, there were a few white colonies, which were proved to be host mutants of 10-22. These mutants were transformable by pIJ702 and homogeneous black colonies were obtained.
Forty-nine cases of the so-called "angioblastic meningioma", six cases of cerebellar hemangioblastoma, and four cases of soft tissue hemangiopericytoma were studied with HE, reticulin stainings, and immunohistochemical reaction with Vimentin, EMA, GFAP, S-100, and UEA-1 antibodies. The results showed that among the three subtypes of "angioblastic meningioma", namely, the hemangiomatous (H), the hemangioblastic (AB), and the hemangiopericytic (P) types, (1) type H belongs to true meningioma; (2) most of type P are almost identical with soft tissue hemangiopericytoma and different from true meningiomas, therefore belong to hemangiopericytoma arising from pericytes; however (3) some true meningiomas may appear as hemangiopericytoma histologically; (4) a few of AB are very similar to cerebellar hemangioblastoma and thus should be considered as supratentorial hemangioblastoma, while most of AB are still true meningiomas.
Trichloroethanol (TCEt) potentiated ion current mediated by 5-hydroxytryptamine (5-HT)3 receptors in isolated adult rat nodose ganglion neurons. The magnitude of potentiation of peak current amplitude increased with increasing TCEt concentrations from 0.5 to 5 mM. The rate of decay of current also increased as a function of TCEt concentration. Steady-state current was unaffected by TCEt at concentrations up to 10 mM. A high concentration of TCEt (25 mM) potentiated peak current but inhibited steady-state current. Potentiation appeared to involve an increase in agonist potency as the magnitude of potentiation of peak current decreased with increasing agonist concentration. Agonist application before TCEt treatment decreased the magnitude of potentiation elicited by 5 mM TCEt. These observations indicate that the potentiating action of TCEt arises from an increase in the efficacy with which 5-HT activates current. TCEt appears to facilitate transitions from closed to open states more readily than transitions from desensitized to open states. These observations are consistent with the hypothesis that 5-HT3 receptor function may contribute to the behavioral pharmacology of alcohols and related sedative/hypnotic agents.
The dorsal (dl) morphogen gradient is responsible for initiating the differentiation of the mesoderm, neuroectoderm and dorsal ectoderm in the Drosophila embryo. dl encodes a sequence-specific DNA binding protein that belongs to the Rel family of transcription factors. Previous studies have shown that dl activates the mesoderm determinant twist (twi); here we use a combination of site-directed mutagenesis and P-transformation assays to demonstrate that it also functions as a direct transcriptional repressor of a second target gene, zerknüllt (zen). By exchanging dl binding sites between the promoters we show that activator sites from twi can mediate repression when placed in the context of the zen promoter, and that repressor sites from zen can mediate activation in the context of the twi promoter. This represents the first demonstration that common binding sites for any DNA binding protein can mediate both activation and repression in a developing embryo. Evidence is also presented that the affinities of dl binding sites are important for the efficiency of repression, but are not the sole determinants of the threshold response to the dl gradient.
In this study, determination of gastrin concentration in bronchoalveolar lavage fluid and serum has been detected by radioimmunoassay in 30 cases of lung cancer and 24 cases of non-cancer pulmonary diseases. The results show that the gastrin concentration and its positive rate of lavage fluids from cancer lung are much higher than those from healthy lung and serum in lung cancer patients, and those from serum and both disease and healthy lung in non-cancer pulmonary disease patients (P less than 0.01). The gastrin ratio of lavage fluids from cancer lung to serum is also significantly higher than the ratio of lavage fluid from healthy lung to serum and all the ratios in the non-cancer pulmonary disease group. These results suggest that there is a high gastrin concentration in local tissue of lung cancer, which is signified by the high concentration of gastrin and its high positive rate in lavage fluids from the lung with cancer. Therefore, the gastrin determination in lavage fluids and gastrin ratio of lavage fluids to serum are more reliable in the differential diagnosis of benign from malignant pulmonary diseases than gastrin determination of serum alone.
Serial changes in serum gastrin level were detected by radioimmunoassay in 58 lung cancer patients before and after operation. In comparing these tests with those of 40 cases of noncancerous thoracic lesions and 151 normal adults, the serum gastrin from lung cancer patients is significantly higher than that of noncancerous thoracic lesions and normal individuals (P less than 0.01). The gastrin level is closely related to stage of cancer, size of primary tumor, presence of lymph node metastasis, and type of histological classification. The serum gastrin was found to decrease gradually after the removal of the tumor and to return to normal on the 14th postoperative day. Those patients whose serum gastrin level can return to normal on the 14th postoperative day will have a good prognosis; if not, their prognosis will be very poor. These results suggest that serum from patients with lung cancer contains a high concentration of gastrin that can help differentiate benign from malignant thoracic lesions and evaluate prognosis of patients with lung cancer. Therefore, the cause of high serum gastrin in patients with lung cancer is likely due to the gastrin-producing property of the lung cancer cells.
1. FK336 (10(-6)-10(-4) M) inhibited contractile responses to norepinephrine (NE), KCl and Ca2+ in isolated rabbit aortas. 2. Relaxing effect of FK336 on KCl-response was inhibited by nitroglycerin (NG), but not by nifedipine or verapamil. 3. FK336 inhibited residual NE response and a subsequent Ca2+ response in Ca(2+)-free medium. FK336 did not affect the inositol monophosphate level. 4. Relaxing effect of FK336 on NE response was inhibited by methylene blue, NG, K(+)-channel inhibitors and acetylcholine (ACh), and potentiated by M&B 22,948 and theophylline. 8-Br cGMP and dibutyl cAMP had no effect. 5. FK336 increased cGMP level in rat aorta. 6. Potentiation of isoproterenol-relaxation by FK336 was inhibited by methylene blue. 7. The inhibitory effect of ACh on FK336-relaxation was eliminated by endothelium removal, nordihydroquaiaretic acid and guinacrine, but not by indomethacin. These treatments themselves did not affect FK336-relaxation. 8. The mode of vasorelaxing action of FK336 is discussed.
D1, a subtype of the dopamine receptors, is widely distributed in the nervous system and has been shown to be positively coupled to adenylate cyclase. Using a combination of in vitro receptor autoradiographic and in situ hybridization techniques, the present study examines the co-distribution of D1 receptor binding sites and D1 receptor mRNA in adjacent rat brain sections. D1 receptor binding sites were labeled using the selective antagonist [3H](R)-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzaz epin- 7-ol (SCH23390) (4.6 nM), in the presence of 1 microM ketanserin, while the D1 receptor mRNA was visualized with a 35S-labeled riboprobe corresponding to a region between transmembrane domains III and VI of the rat D1 receptor (base pairs 383-843). Analysis of serial sections suggested a good agreement between D1 receptor binding and mRNA in several brain regions, including the paleocortex, caudate-putamen, nucleus accumbens, amygdala, and suprachiasmatic nucleus. Marked discrepancies between D1 receptor binding and mRNA were observed in other brain regions including the entopeduncular and subthalamic nuclei, substantia nigra (pars reticulata), hippocampus, and cerebellum. While technical considerations may contribute to these results, much of the discordance between the distributions is probably due to the differential localization of D1 receptor mRNA in cell bodies and receptor binding sites on fibers and may provide insights into receptor synthesis, transport, and membrane insertion. In the basal ganglia, for instance, D1 receptors are synthesized in the striatum and are either transported to efferent projections in areas such as the substantia nigra, or remain localized in striatal cells bodies. Ibotenic acid lesions in the striatum are consistent with these conclusions and demonstrate a coordinate loss of D1 receptor binding and mRNA in the caudate-putamen that is accompanied by a degeneration of fibers projecting to substantia nigra and a loss of D1 binding in the pars reticulata. Neurons in the dentate gyrus and in the granular layer of the cerebellum, on the other hand, synthesize D1 receptors and transport them entirely to either their dendritic or axonal fields, respectively, in the molecular layer. This analysis provides a better understanding of dopaminergic receptor systems in the CNS and their anatomical organization.
Transcription factor IID (TFIID) binds to TATA boxes, nucleating the assembly of initiation complexes containing several general transcription factors and RNA polymerase II. Recently, TFIID was shown to be a multisubunit complex containing a TATA box-binding polypeptide (TBP) and several tightly associated polypeptides (TAFs), which are required for transcriptional stimulation by activator proteins. Here, we report the development of a human cell line expressing an epitope-tagged TBP and the immunopurification of a native, high-molecular-weight form of TFIID that supports transcriptional stimulation by several different classes of activation domains. Recovery of basal and activated TFIID transcriptional specific activity was close to approximately 100%. Electrophoretic mobility-shift analysis demonstrated a single major DNA-protein complex. This holo-TFIID contains TAFs of approximately 250, 125, 95, 78, and 50 kD and sediments at 17S. Holo-TFIID produced an extended footprint over the adenovirus major late promoter TATA box and initiator sequence and supported transcriptional activation from a promoter lacking a TATA box. These results lead us to hypothesize that a single multisubunit TFIID protein supports transcriptional stimulation by diverse activation domains and from a TATA-less promoter.
The vasoinhibitory effect of FK 453 was examined in isolated rabbit aorta. FK 453 inhibited contractile responses to norepinephrine, angiotensin-I and KCl. Pretreatment of the tissue with FK 453 failed to affect the relaxing effect of verapamil on the KCl response and the inhibitory effect of prazosin on the phenylephrine response. FK 453 inhibited both the residual norepinephrine response and the subsequent Ca2+ response in a Ca(2+)-free medium containing EGTA and nifedipine. The inhibitory effect of a combined treatment with either FK 453 plus nitroglycerin or FK 453 plus theophylline, but not with FK 453 plus M & B 22,948 (2-o-propoxyphenyl-8-azapurine-6-one; May & Baker), was much greater than that of any single treatment. Pretreatment with FK 453 also potentiated relaxing effects of nitroglycerin and isoproterenol on the PGF2 alpha response. The effect of a combined treatment with FK 453 plus theophylline, but not with FK 453 plus M & B 22,948, was much greater than that of any single treatment. FK 453 also inhibited the activity of phosphodiesterase from canine aorta to convert cyclic [3H]-GMP and cyclic [3H]-AMP to 5'-GMP and 5'-AMP, respectively. These results suggest that the inhibitory action of FK 453 is not due to inhibition of voltage-operated Ca2+ channels or alpha-adrenoceptors, but due to increase in cyclic GMP level.
In this article, the development of radioimmunoimaging (RII) in China is reviewed. Since 1984 conventional heterologous specific antibodies (Abs), such as anti-carcinoembryonic antigen (CEA) and anti-alphafetoprotein (AFP) Abs, have been used to detect cancers of the colon, ovary, lung, liver, etc. Later on, Abs against specific tumor cell-associated antigens have been produced in many institutions and applied clinically, with quite satisfactory results (detection rate ranging from 80-90%). Recently, human monoclonal antibodies (McAbs) are also being prepared. Finally, the existing problems to be overcome are discussed.
Cultured confluent human umbilical vein endothelial cells were irradiated in vitro with 60Co gamma rays at doses from 0 to 50 Gy. After irradiation thrombomodulin was measured at different times over 6 days in the supernatants of endothelial cell culture medium, on the surface of the cells, and within the cells. At 24 h after irradiation, an increase in the release of thrombomodulin from irradiated endothelial cells and an increase in the number of molecules and the activity of thrombomodulin on the surface of the cells were observed; these reactions were dependent on radiation dose. The capacity of the cells to produce and release thrombomodulin was decreased from 2 to 6 days after exposure to 60Co gamma rays. Our data indicate that radiation can injure endothelial cells, and that thrombomodulin may be used as a marker of radiation-induced injury in endothelial cells. The interrelationship between the dysfunction of irradiated endothelial cells and the pathological mechanisms of acute radiation disease is also discussed.
This paper reports the treatment with Yiqi Huoxue and Shugan Liqi agents in atherosclerosis of rabbit. The results suggested: 1. Both decoctions could reduce the cholesterol of hypercholesterolemia and improve the atherosclerosis, but the former was better than the latter. 2. Both decoctions could alter the components of bile lipids, but on the contrary, the latter was better than the former in reducing the formation of gallstones. 3. Both decoctions could decrease the plasma concentration of LPO and ratio of TXB2/6-K-PGF1 alpha, while increase the ratio of cAMP/cGMP in plasma. So, the different prescriptions of TCM affecting the same link of pathogenesis might play the role of "Different Treatments in Same Disease".
UNLABELLED: Thirty-eight adults including 24 males and 14 females with acute nonlymphocytic leukemia were treated with DATV (Daunorubicin, Cytarabine, 6-thioguaninum, Vincristine) regimen from December 1987 to May 1991. The median age was 31 years old (range 13-54). The DATV regimen consisted of DNR 60 mg/day IV for 3 days; Ara-C 100 mg by continuous infusion every 12 hours for 7 days; 6-TG 150 mg PO for 7 days and VCR 2mg IV on day 1. RESULTS: Complete remission (CR) was achieved in thirty-three of 38 patients after 1-2 courses (mean 1.3) with CR rates 86.8%. Five patients had no response to the regimen. Twenty-four of 33 patients who achieved CR are still in CR for 1-41 months with a median follow-up of 10 months.
Cell cycle phases of bone marrow cells from 8 patients with iron deficiency anemia (IDA), 8 aplastic anemia (AA), 30 myelodysplastic syndrome (MDS), 41 acute leukemia (AL) before treatment, 8 acute leukemia in relapse, 17 acute leukemia in complete remission (CR), 12 chronic myelogenous leukemia (CML) and 4 chronic lymphocytic leukemia (CLL) were analysed with flow cytometry. The proportions of phases of S. G2 M in patients with IDA, refractory anemia, and refractory anemia with ring sideroblast were similar to these in normal controls (P > 0.05). However, they were significantly lower in patients with AA, refractory anemia with excess of blast (RAEB) and transformed RAEB than those in normal controls (P < 0.01, respectively), and CML patients than in normal controls (P < 0.05). The S G2M% was apparently higher in patients with CML than that in CLL (P < 0.01). But, there was no difference between in ALL and ANLL (P > 0.05). It was higher in patients with AL in CR and in relapse than AL before treatment (both P < 0.01). It was still lower in the former than that in normal controls. (P < 0.05). The clinical significance of cell cycle status was also discussed in this paper.
We investigated the effects of neuropeptide Y on the prostacyclin production of cultured porcine aortic endothelial cells by measuring the stable metabolite of prostacyclin, 6-keto-prostaglandin F1 alpha, by radioimmunoassay. Neuropeptide Y induced dose- and time-dependent stimulation of prostacyclin production by cultured porcine aortic endothelial cells. The lowest stimulatory concentration of neuropeptide Y was 10(-8) M and maximal response, a 2.8 fold rise, was obtained with 10(-6) M. The stimulation lasted at least 24 h. The effect was associated with the stimulation of arachidonic acid release. Our data suggest that neuropeptide Y may inhibit the development of atherosclerosis by stimulating prostacyclin synthesis.