Search PubMed⌕ Search

Biomedical subjects

L Qian

Publications and source records attributed to L Qian.

At least 73 records · Page 4Linked to original sources
PubMed1996

Magnetic resonance imaging and pathologic studies on lateral fluid percussion injury as a model of focal brain injury in rats.

In this study, morphologic changes in brain lesions initiated by moderate lateral fluid percussion injury in rats were investigated chronologically using high-resolution magnetic resonance imaging (MRI) and histopathologic methods. Rats were subjected to moderate fluid percussion injury (average 2.80 +/- 0.48 atmospheres) over the exposed dura overlying the right parietal cortex. MRI obtained in vivo were compared with corresponding pathologic findings at 1, 6, and 24 h and at 3, 6, 14 and 80 days after injury. T2-weighted images showed scattered low-signal intensity in the injured cortex within a few hours after injury, whereas histologic findings revealed intraparenchymal hemorrhages. T2-weighted images of the ipsilateral cerebral cortex and/or corpus callosum showed a high-signal-intensity area 4 h after injury. The high-signal-intensity area became largest in size between 6 and 24 h, then declined gradually, and almost disappeared 14 days after injury. Histologic examination revealed pyknosis, retraction of the cell body of neurons with vacuolated neuropil in the corresponding regions 6 and 24 h after injury, and cystic necrosis 14 days after injury. The location and extent of these pathologic changes were depicted accurately by MRI in vivo. In the hippocampus, pyknosis and retraction of the cell body of pyramidal neurons were observed on the injured side 24 h after injury, and the number of neurons in the CA1 and CA2-CA3 regions decreased significantly on the same side by 14 days after injury. It is concluded that morphologic changes in the brain following experimental traumatic brain injury in rats are detectable in vivo by high-resolution MRI, and that MRI may be useful for the evaluation of treatment effects in experimental brain injury.

Animals↗
PubMed1996

Alterations of level of total genomic DNA methylation and pattern of c-myc, c-Ha-ras oncogene methylation in human gastric carcinogenesis.

OBJECTIVE: To investigate the status of DNA methylation in gastric carcinogenesis. METHODS: We analysed methylation pattern of c-myc, c-Ha-ras oncogenes by southern blot hybridization. DNA from cancerous, paracancerous and non-cancerous area of surgically resected samples in 21 cases of advanced gastric cancer were digested with MspI/HpaII and hybridized with the two genomic 32P labelled probes. In addition, the level of total genomic DNA methylation was measured by incubating DNA with 3H-S-Adenosylmethionine (3H-SAM) in the presence of a methylase which methylates all the cytosine residues that are in the double CpG (cytosine-guanine). RESULTS: The results indicated that both c-myc and c-Ha-ras oncogene fragments containing CCGG sequence were hypomethylated in DNA samples from cancerous (10/21 and 5/10) and paracancerous (13/21 and 4/10) areas. Moreover, the level of total genomic DNA methylation in cancerous tissue was significantly lower than that in non-cancerous and paracancerous mucosa tissues (P < 0.05). The results from two methods are incompletely alike. CONCLUSION: These results supported a strong correlation between DNA hypomethylation and gastric carcinogenesis, particularly methylated pattern of c-myc and c-Ha-ras oncogenes fragments containing CCGG sequence was abnormal in gastric mucosa tissue from gastric cancerous and paracancerous areas.

Adult↗
PubMed1995

Saikosaponin A-induced cell death of a human hepatoma cell line (HuH-7): the significance of the 'sub-G1 peak' in a DNA histogram.

Saikosaponin A (SSA) induced cell death in the human hepatoma cell line (HuH-7) was investigated. Shortly after exposure to SSA, a DNA histogram showed a 'sub-G1 peak', which was recently reported as suggestive of apoptosis by other researchers. However, the electrophoresis of DNA indicated that such was not the case in the present experiment. The decreased intake of rhodamine 123 and the swelling of mitochondria were remarkable shortly after SSA exposure. These data seem to support the idea that the sub-G1 peak represents necrosis rather than apoptosis. Interestingly, the DNA electrophoresis revealed the smear pattern of small DNA fragments shortly after SSA-exposure, although it did not show the apoptotic ladder pattern. This finding and the appearance of the 'sub-G1 peak' is thought to have been a result of the degradation of the nuclear DNA in the early stages of cell death. Because these findings are different not only from apoptosis, but also from typical necrosis, a distinct mechanism of cell death caused by SSA is suggested.

Apoptosis↗
PubMed1995

Predominance of a single genotype of Mycobacterium tuberculosis in countries of east Asia.

Analysis of the population structure of Mycobacterium tuberculosis strains from the People's Republic of China showed that the vast majority belong to a genetically closely related group. These strains shared the majority of their IS6110 DNA-containing restriction fragments, and also, the DNA polymorphism associated with other repetitive DNA elements, like the polymorphic GC-rich sequence and the direct repeat, was very limited. Because the majority of these strains originated from the province of Beijing, we designated this grouping the "Beijing family" of M. tuberculosis strains. Strains of this family were also found to dominate in neighboring countries such as Mongolia, South Korea, and Thailand, whereas a low prevalence of such strains was observed in countries on other continents. These data indicate that strains of the Beijing family recently expanded from a single ancestor which had a selective advantage. It is speculated that long-term Mycobacterium bovis BCG vaccination may be one of the selective forces implicated in the successful spread of the Beijing genotype.

China↗
PubMed1995

[Clinical and immunophenotyping features of CD34-positive acute nonlymphoblastic leukemia].

Antigen CD34 and other markers of cell membrane were investigated in cells from 43 patients with primary acute nonlymphoblastic leukemia (ANLL) by immunofluorescence test. The blast cells of 13 patients (30.2%) expressed antigen CD34. The patients with positive CD34 were no significantly different from the remaining 30 patients with negative CD34 with respect to age, serum lactate dehydrogenase (LDH), hemoglobin, white blood cell count, platelet count and the proportion of blast cells in blood and bone marrow, but their blasts were more likely to express HLA-DR, CD38, CD7 and lack of CD15 antigen. These patients had FAB M1 or M5a morphologic characteristics and lower complete remission (CR) rate. This result demonstrated that CD34 positive ANLL is poorly differentiated.

Adolescent↗
PubMed1994

Mcl-1, a member of the Bcl-2 family, delays apoptosis induced by c-Myc overexpression in Chinese hamster ovary cells.

Mcl-1, a protein increased early in the differentiation of human myeloblastic ML-1 cells, has sequence similarity to Bcl-2. In the present study, we determined whether Mcl-1 has functional similarity to Bcl-2 by testing its ability to inhibit apoptosis induced by c-Myc overexpression. This was carried out using Chinese hamster ovary 5AHSmyc cells which contain the human c-myc proto-oncogene under the control of a heat shock promoter. Heat treatment induces c-Myc overexpression and thus apoptosis as determined by internucleosomal DNA fragmentation. We transfected 5AHSmyc cells with mcl-1 and found that clones expressing the introduced Mcl-1 protein exhibited reduced DNA fragmentation. Mcl-1 was also capable of delaying the onset of cell death as judged by loss of membrane integrity, although it could not provide complete protection from c-Myc overexpression. Thus, Mcl-1 has functional homology to Bcl-2 in that Mcl-1 can enhance cell viability under conditions that otherwise cause apoptosis.

Animals↗
PubMed1994

Messenger ribonucleic acid of rat testicular retinoic acid receptors: developmental pattern, cellular distribution, and testosterone effect.

In order to understand the physiological importance and molecular mechanisms of retinoic acid regulation of spermatogenesis, we examined the ontogeny of the steady-state level of the mRNAs of retinoic acid receptor (RAR) alpha and gamma in testes; we also used Northern blot cDNA hybridization to examine the distribution of RAR alpha and RAR gamma in spermatogenic cells isolated from 60-day-old rats. In addition, we investigated the effects of exogenous testosterone on the steady-state levels of mRNA of RAR alpha and gamma in testes of 20-day-old rats. The steady-state levels of both the 3.4- and 2.7-kb mRNA transcripts of RAR alpha in rat testes remained relatively unchanged until 20-21 days of age, then declined thereafter. Comparison of the relative abundance of the RAR alpha transcripts in Sertoli cells isolated from 20-day-old rats with that found in mixed spermatogenic cells isolated from 40-day-old rats suggests that both the 3.4- and the 2.7-kb transcripts were expressed more abundantly in Sertoli cells. Whereas young and pachytene spermatocytes, as well as young and elongated spermatids, all contained the 3.4-kb transcript of RAR alpha, only trace amounts of the 2.7-kb transcript was detected in spermatogenic cells. In addition, trace amounts of a smaller transcript of RAR alpha (1.8 kb) was detected in both Sertoli cells and spermatogenic cells, and two larger transcripts (4.0 and 7.0 kb) were detected exclusively in spermatogenic cells. In contrast, a single 3.4-kb mRNA transcript of RAR gamma was detected in rat testes.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1994

The role of superoxide anions in the pathogenesis of cerebral vasospasm.

BACKGROUND AND PURPOSE: To determine the role of superoxide anions in the pathogenesis of cerebral vasospasm after aneurysmal subarachnoid hemorrhage, we studied the preventive effect of human recombinant copper-zinc superoxide dismutase (h-r SOD) in a rabbit subarachnoid hemorrhage (SAH) model. METHODS: Forty-five rabbits receiving intracisternal injection of 3 mL autologous nonheparinized blood or 3 mL saline were divided into four groups as follows: (1) saline injected and no treatment (control group, n = 6); (2) blood injected and no treatment (SAH group, n = 20); (3) blood injected and treated by multiple intracisternal injections of 30,000 U of h-r SOD in 0.5 mL saline (SOD group, n = 9); and (4) blood injected and treated by multiple intracisternal injections of 0.5 mL saline (saline group, n = 10). Serial angiograms were performed after the blood injection, and the diameter of the basilar artery was measured. Three animals from the control group and five animals from the SAH and SOD groups each were killed 2 days after SAH, and their basilar arteries were processed for transmission electron microscopic observations. RESULTS: In the SAH and saline groups, the diameter of the basilar arteries was significantly reduced (28 +/- 14% and 27 +/- 9%, respectively) at 2 days after the blood injection, then recovered to pre-SAH levels until 11 days. In the SOD group, the diameter of the basilar artery was only minimally changed during the follow-up period. Transmission electron microscopy revealed endothelial injury in all basilar arteries in the SAH group, whereas endothelial injury was minimal in the SOD group. CONCLUSIONS: We determined that h-r SOD prevents the occurrence of vasospasm, possibly as a result of preventing endothelial injury initiated by superoxide anions.

Animals↗
PubMed1994

[Cytogenetic studies on a human cecum adenocarcinoma cell line (HCe-8693)].

Human undifferentiated cecum adenocarcinoma cell line (HCe-8693) was established by Zhejiang Cancer Hospital in 1986. This paper reports the results of cytogenetic studies on the 23rd (early) and 125th (late) passages of this cell line. The numerical distribution range of chromosomes was rather narrow, showing a near diploid karyotype, and no significant difference was observed between early and late passages. The modal number of chromosomes was 49. G-banding karyotypic analysis revealed that the karyotype of this cell line was close to that of normal diploid cells, with few, easily identified abnormal chromosomes. The most significant changes were a distal deletion of the short arm of chromosome No. 1 and a trisomy of chromosome No. 13. The morphological characteristics and possible correlation with pathogenesis of colorectal cancer were briefly discussed.

Adenocarcinoma↗
PubMed1993

T cell receptor-beta mRNA splicing during thymic maturation in vivo and in an inducible T cell clone in vitro.

The expression of TCR-beta mRNAs competent to encode functional V(D)JC beta proteins requires the activation of programmed DNA rearrangement events. It is not known whether other regulatory mechanisms control the steady-state levels of mature TCR-beta transcripts during thymic ontogeny. In this report, we demonstrate that TCR-beta pre-mRNAs accumulate in T cells, thus implicating RNA splicing as another potential level of regulation. Three methods were used to characterize the intron content of these pre-mRNA: Northern blot analysis, ribonuclease H mapping, and reverse transcription polymerase chain reaction analysis. Using these methods, we demonstrate that intron-containing TCR-beta transcripts derived from both the JC beta 1 and JC beta 2 loci accumulate in murine fetal and adult thymus. (VD)JC beta 1 pre-mRNAs that accumulate in the thymus possess unusually long poly(A) tails (> or = 300 nucleotides) and contain different combinations of four introns: the large intron between the J beta 1 and C beta 1 elements and the three introns within the C beta 1 element. The presence of an unusual transcript possessing IVS2C beta 1 at the 5' terminus suggests that cleavage of its splice acceptor is inefficient or negatively regulated. The profile of incompletely spliced TCR-beta transcripts present in the thymus in vivo is identical in intron content to those that we previously showed accumulate in the nucleus of the immature SL12.4 T lymphoma cell clone. An unstable negative regulatory protein may control TCR-beta expression in this cell clone because fully spliced TCR-beta transcripts are dramatically induced in the cytoplasm after treatment with any of five different protein synthesis inhibitors (cycloheximide, anisomyosin, emetine, puromycin, and pactamycin), all of which act by distinct mechanisms to inhibit protein synthesis.

Animals↗
PubMed1993

Quinoxaline N-oxide containing potent angiotensin II receptor antagonists: synthesis, biological properties, and structure-activity relationships.

A series of novel quinoxaline heterocycle containing angiotensin II receptor antagonist analogs were prepared. This heterocycle was coupled to the biphenyl moiety via an oxygen atom linker instead of a carbon atom. Many of these analogs exhibit very potent activity and long duration of effect. Interestingly, the N-oxide quinoxaline analog was more potent than the nonoxidized quinoxaline as in the comparison of compounds 5 vs 30. In order to improve oral activity, the carboxylic acid function of these compounds was converted to the double ester. This change did result in an improvement in oral activity as represented by compound 44.

Administration, Oral↗
PubMed1993

T cell receptor-beta mRNA splicing: regulation of unusual splicing intermediates.

The expression of functional T cell receptor-beta (TCR-beta) transcripts requires the activation of programmed DNA rearrangement events. It is not clear whether other mechanisms dictate TCR-beta mRNA levels during thymic ontogeny. We examined the potential role of RNA splicing as a regulatory mechanism. As a model system, we used an immature T cell clone, SL12.4, that transcribes a fully rearranged TCR-beta gene but essentially lacks mature 1.3-kb TCR-beta transcripts in the cytoplasm. Abundant TCR-beta splicing intermediates accumulate in the nucleus of this cell clone. These splicing intermediates result from inefficient or inhibited excision of four of the five TCR-beta introns; the only intron that is efficiently spliced is the most 5' intron, IVSL. The focal point for the regulation appears to be IVS1C beta 1 and IVS2C beta 1, since unusual splicing intermediates that have cleaved the 5' splice site but not the 3' splice site of these two introns accumulate in vivo. The block in 3' splice site cleavage is of interest since sequence analysis reveals that these two introns possess canonical splice sites. A repressional mechanism involving a labile repressor protein may be responsible for the inhibition of RNA splicing since treatment of SL12.4 cells with the protein synthesis inhibitor cycloheximide reversibly induces a rapid and dramatic accumulation of fully spliced TCR-beta transcripts in the cytoplasm, concomitant with a decline in TCR-beta pre-mRNAs in the nucleus. This inducible system may be useful for future studies analyzing the underlying molecular mechanisms that regulate RNA splicing.

Animals↗
PubMed1992

A spliced intron accumulates as a lariat in the nucleus of T cells.

The vast majority of mammalian genes are interrupted by non-coding segments of DNA termed introns. Introns are spliced out of RNA transcripts as lariat structures, and then are typically debranched and rapidly degraded. Here, we described an unusual spliced intron from the constant region of the T cell receptor-beta (TCR-beta) locus that is relatively stable in mammalian cells. This intron, IVS1C beta 1, accumulates as a set of lariat RNA structures with different length tails in the nucleus of T cells. The accumulation of this spliced intron is developmentally regulated during murine thymocyte ontogeny. The property of stability appears to be evolutionarily conserved since the human version of this intron also accumulates in T cells. The stability is selective since other spliced TCR-beta introns do not detectably accumulate in T cells. The unusual stability of this intron does not depend on T cell specific factors since non-T cells transfected with TCR-beta gene constructs also accumulate spliced IVS1C beta 1. The discovery of a mammalian intron that accumulates as a lariat in vivo provides an opportunity to elucidate mechanisms that regulate intron debranching, stability, and nuclear localization.

Animals↗
PubMed1992

The role of nuclear medicine in oncology.

Nuclear Medicine offers screening methods for oncology such as bone and bone marrow scintigraphy. During the last two decades, special procedures have gained widespread application. This paper is centered around the "tumor-specific" radiopharmaceuticals. In patients with thyroid cancer, I-131 still plays a significant role. Ga-67 still has its indications in lymphoma, while in other diseases Tl-201 chloride is now the agent of choice. Especially in thyroid cancer, Tl-201 has proved to be a reliable tumor imaging radiopharmaceutical. More recently, Tc-99m MIBI was introduced for tumor imaging. Tc-99m HMPAO may also be used for tumor scintigraphy, especially in brain lesions. In addition, I-123 IMP has successfully been used for imaging malignant melanoma. Another promising field of tumor diagnosis is receptor imaging. In neuroblastoma and malignant pheochromocytoma, I-131/123 mIBG is the radiopharmaceutical of choice and may be considered as a receptor imaging agent also. First clinical results with In-111 octreotide show potentials as somatostatin-receptor radiopharmaceutical in insulinoma, islet cell carcinoma, medullary and lung cancer, while I-123 estradiol needs some improvement until it may be recommended as diagnostic tool in breast cancer. Since 1978, radiolabeled poly- or monoclonal tumor antibodies and their fragments have gained widespread application. Especially the Tc-99m 225.28S melanoma antibody, I-131 or Tc-99m CEA and In-111/I-131 labeled OC-125 antibodies have proven to be of clinical significance in melanoma, colorectal and ovarian cancer.

Gallium Radioisotopes↗
PubMed1992

TcR-alpha mRNA accumulation does not dictate cell surface TcR/CD3 expression.

The TcR-alpha chain is the last subunit of the TcR/CD3 complex to be expressed during thymic ontogeny. Since the presence of all subunits are required for efficient expression of this complex on the cell surface, this has lead to the hypothesis that the TcR-alpha chain is the limiting subunit which controls cell surface TcR/CD3 expression during thymocyte differentiation. We have examined this issue using a T-lymphoma cell clone, RS4.2, which has a CD4- CD8- Thyl+ J11d+ IL2R+ phenotype, identical with immature thymocytes which have the capacity to generate all major T cell subsets. The RS4.2 cell clone accumulates abundant amounts of TcR-beta, CD3-gamma, -delta, -epsilon and -zeta transcripts, but expresses trace levels of TcR-alpha transcripts and cell surface TcR/CD3. TcR-alpha mRNA levels can be dramatically augmented in RS4.2 cells by three distinct mechanisms: in response to treatment with either phorbol myristate acetate (PMA), calcium ionophore (A23187), or cycloheximide (CHX). However, the expression of TcR/CD3 on the cell surface fails to be increased by any of these agents. In fact, PMA induces a rapid down-regulation of cell surface TcR/CD3 expression. In contrast, these agents trigger an increase in cell surface IL2R expression which coincides with augmented IL2R-alpha mRNA levels. Thus, in RS4.2 cells, IL2R surface expression is controlled by transcript levels, while TcR/CD3 surface expression is regulated by post-transcriptional events, independent of TcR-alpha mRNA accumulation.

Antigens, Differentiation, T-Lymphocyte↗