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S X Jiang

Publications and source records attributed to S X Jiang.

At least 19 recordsLinked to original sources
PubMed2001

Hyalinizing spindle cell tumor with giant rosettes: report of a case showing remarkable myofibroblastic differentiation.

We examined the proliferative activity and the differentiation line of tumor cells in a case of "hyalinizing spindle cell tumor with giant rosettes" (HSCGR). A 6 cm tumor within the right deltoid muscle of a 58-year-old female was found by physical and radiographical examinations. A biopsy revealed the histological features of a spindle cell tumor with rosette-like structures. Wide excision was done under the diagnosis of HSCGR. The tumor presented as a gray-whitish, solid mass with focal pseudocystic degeneration. Immunohistochemically, the tumor cells were diffusely positive for vimentin and were also focally positive for S-100, but negative for desmin and alpha-smooth muscle actin. The cells stained positively for Ki-67 with even distribution, there being a correlation with the cellularity of the areas, with a labeling index ranging from 0.3 to 0.5%. In addition, flow cytometry revealed an almost normal diploid DNA pattern and 5.8% S-phase fraction, indicating low proliferative activity. Ultrastructurally, many tumor cells displayed discontinuous basal lamina, pinocytotic vesicles, dilated rough endoplasmic reticulum, and microfilaments with focal dense bodies. The main component of the rosette was collagenous fibrils with normal diameter and normal periodic banding. We interpreted this case of HSCGR as a low grade fibrosarcoma with remarkable differentiation of myofibroblastic lineage, and with focally accumulated, morphologically normal collagenous fibrils.

Cell Differentiation↗
PubMed2001

Antitumor effect of bcl-2 antisense phosphorothioate oligodeoxynucleotides on human renal-cell carcinoma cells in vitro and in mice.

BACKGROUND AND PURPOSE: Programmed cell death is a genetically regulated pathway that is altered in many cancers. This process is, in part, regulated by the bcl-2 oncogene. Antisense oligodeoxynucleotides (ODNs) targeted to specific oncogenes have been used with some therapeutic success in animal models of leukemia and melanoma cells and human Hodgkin's lymphoma. We evaluated the effects of antisense ODNs targeted to the bcl-2 oncogene on the proliferation of human renal-cell carcinoma (RCC) cells in vitro and on the growth of human RCC xenografts in BALBc nude (nu/nu) mice. MATERIALS AND METHODS: Expression bcl-2 mRNA in five RCC cell lines (ACHN, Caki-1, RCZ, RCW, and OS-RC-2) was analyzed by reverse transcriptase-polymerase chain reaction. The effects of phosphorothioated ODNs containing human bcl-2 sense and bcl-2 antisense sequences that were transfected with Lipofectin on the proliferation and viability of cultures of established human RCC cell lines were determined by MTS assay. The expression of Bcl-2 protein in ACHN tumor cells following antisense bcl-2 (AS2) ODN treatment was evaluated by Western blot analysis, and the extent of apoptosis in these cells was determined by fluorescence-activated cell sorter (FACS) analysis. The antitumor activity in ACHN xenografts in nu/nu mice was monitored by measuring differences in tumor weight in treated and control mice. RESULTS: Expression of bcl-2 mRNA was detected in all five RCC lines. Treatment with antisense bcl-2 ODNs inhibited the growth of all tested RCC cells and decreased Bcl-2 protein expression in ACHN cells. The AS2 antisense ODN complementary to the coding region of bcl-2 mRNA showed a superior antiproliferative effect compared with AS1 ODN complementary to the translation initiation region. Inhibition by antisense bcl-2 ODNs of ACHN cells was dose dependent. The FACS analysis revealed that growth inhibition was associated with the induction of programmed cell death. In vivo, AS2 ODN antitumor activity was noted in locally injected groups. CONCLUSIONS: Treatment of human RCC with antisense ODNs targeted to bcl-2 inhibits growth and is associated with the induction of programmed cell death. These results suggest therapeutic use of antisense bcl2 in the treatment of RCC.

Animals↗
PubMed2001

[Study on analysis of concentration of surfactant PS in injected-produced liquor used in ASP flooding with HPLC].

Ion exchanger and ODS bonded silica gel for HPLC packing were prepared. An HPLC method for the analysis of surfactant PS concentration in injected-produced liquor has been established to meet the need of ASP flooding developed in Gudao West Block of Shengli Oilfield, with a minimum detectable limit of 0.4 mg/L, a linear range of 50 mg/L-1,000 mg/L and recoveries of 95.7%-99.8%. This method has provided great technical support in a variety of fields to the design of the prescription for ASP flooding, the regulation of injection measurement, the quality control of products and the study on the mechanism of oil flooding etc.

English Abstract↗
PubMed2000

Effect of experimental fasciolosis on antipyrine metabolism and clearance in water buffaloes.

The effect of chronic Fasciola hepatica infection on the metabolism of antipyrine, a marker of microsomal oxidative metabolism, was investigated in male water buffaloes dosed daily with 60 F. hepatica metacercariae over 20 days. The plasma elimination half-life of antipyrine was significantly elevated by 23% at 11 weeks postinfection (p.i.) but did not significantly differ from the control period at 20 weeks p.i. The systemic clearance of antipyrine decreased by 48% at 11 weeks p.i. and then returned to normal. The renal clearance for each of the main antipyrine metabolites decreased at 11 weeks p.i. (hydroxymethylantipyrine (HMA), -42%; norantipyrine (NORA), -58%; and 4-hydroxyantipyrine (OHA), -70%) and did not significantly differ from the control period at 20 weeks p.i. These findings indicate that experimental subclinical fasciolosis leads to altered antipyrine kinetics and to an inhibition of the different antipyrine metabolic pathways in water buffaloes.

Animals↗
PubMed2000

Relationship between p53 gene mutation and protein expression: clinical significance in transitional cell carcinoma of the bladder.

Although the mutated p53 gene has been postulated to induce immunohistochemically-detectable p53 protein, reports regarding the relationship between p53 mutation and p53 protein expression have been contradictory. This study investigated the relationship between p53 mutations and p53 expression and their clinical significance for patients with transitional cell carcinoma of the bladder. Eighty-seven transitional cell carcinoma of the bladder were analyzed by immunohistochemistry (IHC) for p53 nuclear accumulation, and the results compared to mutations detected in the p53 gene evaluated by polymerase chain reaction single-strand conformation polymorphism (SSCP) and DNA sequence analysis. By p53 IHC analysis, positive p53 staining was observed in 50 (57.5%) of the 87 tumors. The specificity of IHC, defined as a percentage of IHC negative (<20%) tumors among tumors without mutation, was 94.6%. Despite the good concordance between p53 mutation and p53 protein expression (p<0.0001), 48.0% (24/50) of the tumors showed p53 overexpression without mutation, and 2 (5.4%) tumors with mutation showed no p53 immunoreactivity. Patients with higher grade (grade 3), stage (stages pT2-4), and p53 mutations had a poorer prognosis by Kaplan-Meier survival analysis. A Cox univariate analysis found that grading (hazard ratio 3.139; p=0.002), staging (hazard ratio 3.832; p=0.0005) and p53 mutation (hazard ratio 2.498; p=0.013) were significant variables in these patients, but no variable was independently associated with an increased survival of bladder carcinoma by multivariate analysis. We found that a 20% cut-off level of p53 overexpression showed the highest correlation with prognosis and p53 mutation, however, p53 overexpression and mutation were not superior to staging as prognostic markers. These data suggest that careful assessment of the TNM staging system remains the most reliable predictive indicator of survival for patients with transitional cell carcinoma of the bladder.

Adult↗
PubMed2000

[Chiral separation of glycerin monosulfides and bisulfides with a stationary phase of amylose-tris(3,5-dimethylphenylcarbamate)].

Amylose-tris(3,5-dimethylphenylcarbamate) (ADMPC) and aminopropylated silica gel(APS) were prepared after the reported methods. ADMPC was immobilized on APS from tetrahydrofuran solution with a coating amount of 15%. The chiral stationary phase was packed in a stainless-steel column(150 mm x 4.6 mm i.d.) by slurry method. The column was used for the enantioseparation of 6 glycerin monosulfides and 4 glycerin bisulfides. Mixtures of hexane and 2-propanol were used as mobile phases. The enantiomers of the monosulfides could be separated quite well, while those of the bisulfides could not at all. This phenomenon shows that the ether oxygen atom of the monosulfides plays a key role in the chiral discrimination process. The retention time of the solutes increases significantly as the amount of 2-propanol decreases. This shows the main interaction between the solutes and the chiral stationary phase is hydrogen bonding. A dynamic model is presented to account for the chiral discrimination mechanism.

Amylose↗
PubMed2000

[Direct optical resolution of acidic biphenyl drugs by high performance liquid chromatography on tris(3,5-dimethylphenylcarbamate) of cellulose].

A chiral stationary phase was prepared by coating cellulose-tris(3, 5-dimethylphenylcarbamate) onto aminopropylated silica gel. A series of enantiomeric acidic biphenyl drugs were directly resolved on the chiral stationary phase (CSP) by normal-phase high performance liquid chromatography (HPLC). A hexane-2-propanol eluting system containing 1% of trifluoroacetic acid was used as mobile phase. Efficient optical resolution of the acidic biphenyl drugs has been attained. The factors that influence chiral discrimination such as structural characeristic of the samples and mobile phase were investigated. An interaction model between the stationary phase and the samples was discussed. The results showed that efficient optical resolution of racemic carboxylic acids could be attained by normal-phase HPLC on CSP using a hexane-2-propanol eluting system containing 1% of trifluoroacetic acid.

Carbamates↗
PubMed1999

Tumor extension and cell proliferation in adenocarcinomas of the lung.

To elucidate the mechanism of tumor extension in human pulmonary adenocarcinoma, we immunohistochemically investigated the expression of cell cycle regulator proteins in 54 small adenocarcinomas less than 3 cm in diameter. The Ki-67-labeling index was significantly higher in the periphery of the tumor nodule than in the center. This proliferative potential correlated well with coexpression of cdk2 and cyclin A. p27, one of the cdk inhibitors, was highly expressed in normal bronchial epithelial cells. Peripherally located tumor cells expressed p27 at an intermediate level, but at a higher frequency and level than those in the center. Expression of p21 was also predominant in the periphery. Furthermore, the expression patterns of p21 and p27 were reciprocal. In vitro kinase assays further demonstrated higher cdk2 kinase activity in the periphery. These results suggest that: (i) within an emerging extension made up of peripherally located tumor cells, their high proliferative potential gradually wanes as their relative topographical position becomes more central in the expanding tumor; (ii) peripherally located tumor cells maintain their proliferative potential by higher cyclin A-cdk2 complex activity; and (iii) intermediate expression of p21/p27 in the peripherally located cells promotes higher cyclin A-cdk2 kinase activity, whereas high p21/p27 expression in nonneoplastic cells inhibits kinase activity.

Adenocarcinoma↗
PubMed1999

The significance of frequent and independent p53 and bcl-2 expression in large-cell neuroendocrine carcinomas of the lung.

Both p53 and bcl-2 genes are involved in regulating cell death. Reports, however, concerning the relationship between p53 and bcl-2 expression are contradictory. Large-cell neuroendocrine carcinoma (LCNEC) of the lung is a newly recognized clinicopathologic entity. p53 mutation and bcl-2 overexpression are frequent in small-cell lung carcinoma (SCLC), and we observed a close correlation between bcl-2 expression and cellular neuroendocrine (NE) differentiation in non-SCLC, so we speculated that LCNEC, an NE tumor closely related to SCLC, would exhibit high incidence of both p53 alteration and bcl-2 expression. Immunohistochemical expression of p53 and bcl-2 was evaluated on consecutive sections of 26 LCNECs, including 4 combined LCNECs. p53 accumulation and diffuse bcl-2 staining were observed in 18 (69.2%) of 26 and 24 (92.3%) of 26 LCNECs, respectively, but their immunoreactivities showed no fixed distribution relevance on consecutive sections in individual tumors. Statistical analyses yielded no relationship between p53 and bcl-2 expression (P = .47). In all of the four combined LCNECs, p53 was identically either positive or negative in both tumor cell populations with and without NE differentiation. bcl-2 immunoreactivity was observed only for the tumor cells with NE phenotype in three of the four combined LCNECs and was diffuse among the NE tumor cells but geographic in distribution among the non-NE tumor cells of the remaining one combined LCNEC. Thus, our present findings suggest that p53 and bcl-2 are expressed independently and might have distinct expression significance in LCNECs. A high incidence of p53 expression in LCNECs and equal p53 expression profiles in NE and non-NE tumor cell populations of combined LCNECs suggest that p53 alteration is primarily involved in the tumorigenesis of LCNEC. On the other hand, frequent bcl-2 expression in pure LCNECs and selective bcl-2 expression in tumor cells with NE phenotype in combined LCNECs are suggestive of a role for bcl-2 in regulating cellular NE differentiation.

Carcinoma, Neuroendocrine↗
PubMed1998

Active cyclin A-CDK2 complex, a possible critical factor for cell proliferation in human primary lung carcinomas.

Expression of cyclins A and E and cyclin-dependent kinase 2 (CDK2) was examined immunohistochemically in 190 cases of human lung carcinoma. Cyclin A and CDK2 were expressed in the majority of squamous cell carcinomas, small cell carcinomas, and large cell carcinomas, but in significantly fewer cases of adenocarcinomas. Cyclin E was expressed in a minority of all subtypes. In particular, well differentiated cells in squamous cell carcinoma stained positively for cyclin E; in contrast, cyclin A was expressed in the nonkeratinized proliferating areas of the tumor nests. Immunoblotting revealed that all these proteins were expressed at higher levels in tumor tissues than in adjacent normal tissues. Immunoprecipitation also revealed higher levels of cyclin A and cyclin E associated with CDK2 in tumor tissues. Furthermore, tumor tissues which exhibited higher cyclin A and CDK2 expression also had higher CDK2 kinase activity. However, cyclin E-associated kinase activity was barely detectable even in tumor samples exhibiting higher cyclin E expression. Consistent with these data, elevated expression of cyclin A correlated to shorter survival periods in contrast to expression of cyclin E, which correlated to longer survival periods. These results suggest that in human lung carcinomas, elevated expression of active cyclin A-CDK2 complexes with associated higher CDK2 kinase activity is critical for promoting cell cycle progression and unrestrained proliferation of tumor cells and can be a predictive marker for patients' prognosis. On the other hand, immunohistochemical detection of cyclin E-CDK2 reflects accumulation of inactive forms of protein complexes, implying differentiation or senescence of the tumor and the better prognosis.

Adenocarcinoma↗
PubMed1998

Large cell neuroendocrine carcinoma of the lung: a histologic and immunohistochemical study of 22 cases.

Large cell neuroendocrine carcinoma (LCNEC) of the lung is defined as a poorly differentiated and high-grade neuroendocrine tumor that is morphologically and biologically between atypical carcinoid and small cell lung carcinoma (SCLC). During a survey concerning bcl-2 protein expression in the subtypes of lung cancer, we noticed that two previously diagnosed non-SCLCs met the criteria for LCNEC. Because LCNEC is a newly recognized clinicopathologic entity and because all reported cases have been retrieved from the so-called "neuroendocrine tumor file," we suspected that LCNEC had been underdiagnosed. In the present study, we histologically reviewed 766 surgically resected lung cancers and were able to diagnose 22 (2.87%) LCNECs with the neuroendocrine features subsequently confirmed by immunostaining for multiple neuroendocrine markers. Each case stained positively for at least three general neuroendocrine markers, and 12 (54.5%) also were positive for neuroendocrine hormones. Histologically, most LCNECs showed a marked decrease in or a loss of organoid architecture and could be mistaken for poorly differentiated adenocarcinoma or squamous cell carcinoma. Because our LCNECs are the first to be identified by retrospective review of routinely diagnosed lung cancers, and 18 had been classified as non-SCLC, they may represent cases relatively difficult to diagnose. The present study shows that the most difficult diagnostic factor of LCNEC is the recognition of its light microscopic neuroendocrine features, and LCNEC must be distinguished not only from atypical carcinoid or SCLC, but also from common non-SCLC. Histologically, when an organoid architecture is subtle or absent, the rosettelike structure becomes the best marker for the recognition of neuroendocrine differentiation. Clinically, the prognosis for our LCNECs was significantly worse than that for stage-comparable non-SCLCs (p = 0.046).

Aged↗
PubMed1996

Bcl-2 protein expression in lung cancer and close correlation with neuroendocrine differentiation.

For determination of the cellular distribution of bcl-2 expression in lung cancer and clarification of its correlation with cell neuroendocrine differentiation, Bcl-2 immunostaining was carried out on a large series of formalin-fixed, paraffin-embedded lung cancer samples, and four general neuroendocrine marker and seven peptide hormone stainings were carried out on all Bcl-2-positive squamous cell carcinomas and adenocarcinomas of the lung as well as on 8 pulmonary neuroendocrine carcinomas histologically diagnosed. In addition, 3 small cell lung cancer cell lines were studied by Western blotting. Neuroendocrine differentiation in Bcl-2-negative squamous cell carcinomas and adenocarcinomas was examined with chromogranin A and alpha-subunit of Go protein stainings. Bcl-2 protein was detected in 104/111 small cell carcinomas, 8/8 neuroendocrine carcinomas, 0/6 typical (well differentiated) carcinoids, 23/64 squamous cell carcinomas, 4/65 adenocarcinomas, and all 3 small cell lung cancer cell lines. All 8 neuroendocrine carcinomas, 11 of the Bcl-2-positive squamous cell carcinomas, and all 4 Bcl-2 positive adenocarcinomas expressed multiple neuroendocrine markers. The distributions of Bcl-2 and neuroendocrine marker immunoreactivity closely paralleled each other on consecutive sections. In squamous cell carcinomas, Bcl-2-positive cells could be roughly subdivided into those with neuroendocrine differentiation features, usually demonstrating intense Bcl-2 staining, with basaloid tumor cells usually expressing weak to moderate Bcl-2 staining. The present study clearly shows Bcl-2 protein expression to be remarkably differentially regulated according to histological types of lung cancers and to appear to quite likely be closely associated with neuroendocrine differentiation of tumor cells, indicating that bcl-2 is importantly involved in cell development and differentiation, in addition to protecting cells from apoptosis. Bcl-2 might be usable as a neuroendocrine marker in lung cancers and possibly also in neural-crest-derived tumors.

Adenocarcinoma↗
PubMed1995

Expression of bcl-2 oncogene protein is prevalent in small cell lung carcinomas.

To investigate the frequency of bcl-2 oncogene protein expression in small cell lung carcinoma (SCLC), immunohistochemical staining with a mouse-anti-human monoclonal antibody, bcl-2/124, was carried out on 60 formalin-fixed, paraffin-embedded SCLC samples obtained from surgical biopsy, and autopsy cases. bcl-2 protein was detected in 54 out of the 60 SCLCs. In 47 cases, more than half of the tumour cells stained positively. The staining intensity of the tumour cells was comparable to that of infiltrating lymphocytes in 37 cases, but varied from area to area and even from cell to cell. Negative data in six cases were found to be due to unsuitable fixation or embedding procedures rather than the absence of the antigen. bcl-2 oncogene protein may thus be expressed in most if not all SCLCs. bcl-2 may have potential diagnostic and therapeutic importance in SCLCs and non-SCLCs. Previous cytogenetic and molecular genetic analyses indicate that SCLCs carry a number of chromosomal abnormalities and it would follow from the present results that the abnormal expression of bcl-2 may also play a role in the pathogenesis of SCLC, by increasing tumour mass through inhibition of apoptosis as previously proposed. The diagnostic, prognostic, and therapeutic implications of these findings should be studied in greater detail.

Carcinoma, Small Cell↗
PubMed1992

Effects of the stem cell factor, c-kit ligand, on human megakaryocytic cells.

The kit ligand (KL), also termed stem cell factor (SCF), is a recently discovered hematopoietic growth factor that augments response of early progenitor cells to other growth factors and supports proliferation of continuous mast cell lines. Histological studies suggest that the receptor for SCF/KL, the c-kit proto-oncogene product, is present in bone marrow megakaryocytes. We studied the effects of SCF/KL on immortalized human megakaryocytic cell lines (CMK, CMK6, and CMK11-5) and on isolated human marrow megakaryocytes. Human SCF/KL alone or in combination with the hematopoietic growth factors, interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-6, stimulated proliferation of these megakaryocytic cell lines. SCF/KL treatment did not alter expression of gpIb, gpIIb/IIIa, LFA-1, ICAM-1, or GMP-140 in CMK cells. No effect on ploidy was observed. Furthermore, human SCF/KL induced expression of IL-1 alpha, IL-1 beta, IL-2, and IL-6 in CMK cells. In a fibrin clot system, SCF/KL modestly potentiated megakaryocyte colony formation when added alone to cultures containing CD34+, DR+ bone marrow cells. Addition of SCF/KL with IL-3 or GM-CSF to these cultures resulted in a more marked marrow megakaryocytic cells. SCF/KL may directly affect megakaryocytopoiesis, as well as secondarily modulate hematopoiesis through induction of cytokines in target cells.

Antigens, Surface↗
PubMed1991

[A study on the cellular heterogeneity of lung carcinoma].

The cellular heterogeneity and histological origin of 28 cases of lung carcinoma were studied by light and electron microscopy, as well as by immunohistochemical technique. Most and possibly all of the lung carcinomas were heterogeneous. In 5 of these cases, dual-differentiation in individual cells was revealed. It seems that various types of primary lung carcinoma, including small cell carcinoma, have the same histogenesis. Neuro-endocrine differentiation is not only seen in the typical small cell carcinoma, but is also seen in other types of lung carcinoma.

Adenocarcinoma↗
PubMed1989

[Studies on endotoxin of Leptospira. V. The effect of EDTA-Na on the release of the LPS of Leptospira interrogans serovar lai].

The yield of leptospiral LPS was able to increase 1-2 times when the cells were treated with EDTA-Na before extracting with hot phenal-water method. The colours and solubility of L-LPS were improved. When the leptospiral cells were stored for a long period of time, and treated by EDTA-Na, the phase distribution of the LPS changed, i.e. they returned from water phase into phenol phase. Such change was related to the quantity of both the saccharide and lipid.

Edetic Acid↗