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Biomedical subjects

C Mao

Publications and source records attributed to C Mao.

At least 127 records · Page 7Linked to original sources
PubMed1996

[Expression of p53 gene in oral squamous cell carcinoma and its relations with clinical and pathological parameters and prognosis of patients].

One hundred and eleven cases of oral squamous cell carcinoma (OSCC) were examined for overexpression of p53 protein by using immunohistochemical technique. Association of p53 protein overexpression with clinical and pathological parameters as well as prognosis of patients were also analyzed, p53 protein overexpression was commonly observed (69.4%) in the OSCC patients and might be used as a marker of carcinogenesis of OSCC. The level of p53 protein overexpression was correlated with the decreased three and/or five-year survival rate of OSCC. The presence of p53 was not correlated with patient's sex and age, site and size of tumor, degree of differentiation, node status or clinical stage of OSCC. Single factor COX proportional hazards regression model analysis indicated that there was no significant relationship between p53 overexpression and prognosis of OSCC. Multivariable COX model analysis failed to establish effective life function or risk rate function. This showed that all the parameters analyzed in this study as well as p53 overexpression were not significant or effective risk factors to predict prognosis of OSCC patients.

Adult↗
PubMed1995

DNA binding specificities of Spi-1/PU.1 and Spi-B transcription factors and identification of a Spi-1/Spi-B binding site in the c-fes/c-fps promoter.

Spi-1/PU.1 and Spi-B encode hematopoietic-specific transcription factors that are the most distantly related members of the Ets family. The Ets proteins share a conserved 85 amino acids DNA binding domain, the Ets domain and recognize various DNA target sites around a common core 5'-GGAA/T-3'. The DNA binding specificities of Spi-1 and Spi-B were investigated by using the method of polymerase chain reaction (PCR)-mediated random site selection. The deduced Spi-1 and Spi-B consensus binding sites are very similar suggesting that the functional activities of Spi-1 and Spi-B cannot be distinguished on the basis of their DNA binding specificities. We identified a putative Spi-1/Spi-B binding site in the promoter region of the c-fes/c-fps protooncogene which encodes a tyrosine kinase expressed predominantly in myeloid cells. In vitro translated Spi-1 and Spi-B proteins were capable to bind this site similarly and to activate the c-fes promoter in HeLa transfected cells. We showed that Spi-1 binds the Spi-1/Spi-B binding site of c-fes in HL-60 cells suggesting that Spi-1 may be involved in the regulation of c-fes transcription in myeloid cells. Intriguingly, we detected only Spi-1 binding to this site in the Raji cell line which express both Spi-1 and Spi-B proteins. This suggests that Spi-1 and Spi-B exhibit different DNA binding activities in vivo although they share similar DNA binding specificities in vitro.

Animals↗
PubMed1995

Atomic structure at 2.5 A resolution of uridine phosphorylase from E. coli as refined in the monoclinic crystal lattice.

Uridine phosphorylase from E. coli (Upase) has been crystallized using vapor diffusion technique in a new monoclinic crystal form. The structure was determined by the molecular replacement method at 2.5 A resolution. The coordinates of the trigonal crystal form were used as a starting model and the refinement by the program XPLOR led to the R-factor of 18.6%. The amino acid fold of the protein was found to be the same as that in the trigonal crystals. The positions of flexible regions were refined. The conclusion about the involvement in the active site is in good agreement with the results of the biochemical experiments.

Amino Acid Sequence↗
PubMed1995

Observations on the developmental patterns and the consequences of pancreatic exocrine adenocarcinoma. Findings of 154 autopsies.

OBJECTIVE: To improve our future care of the patient with exocrine pancreatic cancer by seeking, within the limitations of our present approaches, additional information on the growth and spread of the cancer and its influences on the patient. DESIGN: Consecutive autopsies of all patients with exocrine pancreatic cancer were reviewed retrospectively by two surgeons and three pathologists. SETTINGS: Three teaching hospitals of the Medical College of Ohio, Toledo. MATERIALS: One hundred fifty-four consecutive autopsies of patients with exocrine pancreatic cancer during the period between 1952 and 1992. RESULTS: Intrapancreatic metastases or multicentric cancers were found in 12 patients. In 32 patients, pancreatic cancer skipped the lymph nodes, primarily draining the respective areas of the pancreas to metastasize to the secondary chain of nodes. In 13 patients, pulmonary metastases occurred without hepatic metastasis. Intrapancreatic contiguous extension was identified in 34 patients. Carcinoma of the body and/or tail of the pancreas was characterized by transperitoneal as well as hematogenous dissemination to a greater extent than was carcinoma of the head of the pancreas. Seven of 11 small tumors (< 2 cm in diameter) were associated with remote metastases. Relatively severe chronic obstructive pancreatitis was found to have resulted from pancreatic carcinoma in 18 cases, whereas in seven patients, pancreatic carcinoma probably developed in preexisting chronic pancreatitis. Thromboembolic disease was found in 30 patients, more frequently in the patients with the mucin-producing tumors of the pancreatic body and tail. In 21 patients, the amount of ascites was not proportional to the severity of peritoneal dissemination, vessel invasion, or recognizable hepatic dysfunction. Thromboembolic disease, severe infection, stress ulcer, and acute hemorrhagic erosive gastroenteritis were frequent systemic complications contributing to death. Malnutrition in the form of cachexia was undoubtedly a major, even dominant, feature in many patients that could not be quantitated from this data. CONCLUSIONS: Metastasizing cells frequently bypass the initial filters in lymph nodes, liver, or lung to become established in secondary or tertiary sites. Intrapancreatic metastases or multicentric tumors also may develop more frequently than generally has been recognized. Small cancers (< 2 cm in diameter) are often associated at autopsy with remote metastases. These facts would appear to limit the usefulness of the current staging of resected cancers of the pancreas. Cancers of the body or tail are characterized by transperitoneal and hematogenous spread to a greater extent than are those of the head. Anatomical studies often do not explain the cause or the extent of ascites associated with pancreatic adenocarcinoma. As previously indicated, chronic pancreatitis appears to be further confirmed as a precursor of pancreatic cancer.

Adenocarcinoma↗
PubMed1995

Von Recklinghausen's disease associated with duodenal somatostatinoma: contrast of duodenal versus pancreatic somatostatinomas.

A case of Von Recklinghausen's disease with duodenal somatostatinoma is reported. A search of the world's literature revealed 27 patients with Von Recklinghausen's disease associated with an immunohistologically proved duodenal somatostatinoma. Twenty-nine cases of duodenal somatostatinoma not associated with Von Recklinghausen's disease and 32 cases of pancreatic somatostatinomas have been identified for comparison. While their histology may be similar in many respects, the duodenal and pancreatic somatostatinomas show significant differences, especially in hormonal and growth behaviors. In contrast to its pancreatic counterpart, the duodenal somatostatinoma is frequently associated with Von Recklinghausen's disease, is seldom associated with a recognizable "somatostatin syndrome," often contains psammoma bodies, and is less frequently associated with demonstrable metastases at the time of operation.

Adult↗
PubMed1995

Malignant islet cell tumor associated with hypercalcemia.

BACKGROUND: Three cases of islet cell tumors of the pancreas with hypercalcemia were studied, and 16 similar cases have been found in a 25-year review of the English-language literature. The purpose of the study was to review the cause of the hypercalcemia and the clinical characteristics of the tumors. METHODS: Tumor tissue retrieved from paraffin-embedded blocks was studied immunohistochemically for both parathyroid hormone (PTH) and PTH-related protein (PTHrP). PTH was measured in the serum in each patient and the serum PTHrP was measured by immunoassay in one patient. RESULTS: One of our patients had a fatal serum calcium level of 26.4 mg/dl. PTHrP stains were positive in two of our tumors, and one patient had an elevated PTHrP serum level. Serum PTH levels were normal or low in each patient. All three tumors were malignant and extremely vascular. The total group of 19 patients have in common hypercalcemia associated with a normal or low serum PTH level. Although the cause of hypercalcemia has not been proved, the tumors apparently produce PTHrP, because seven of eight tumors stained positive for PTHrP and each of the four patients tested had an elevated PTHrP serum titer. The tumors are extremely vascular, are usually malignant (17 of 18), and become large, but they are compatible with a relatively long patient survival time. CONCLUSIONS: These neuroendocrine tumors associated with hypercalcemia share several characteristics, but a claim that they represent another type of "functioning islet cell tumor" should await a clearer delineation of the cause of the hypercalcemia.

Adenoma, Islet Cell↗
PubMed1995

Papillary cystic and solid tumors of the pancreas: a pancreatic embryonic tumor? Studies of three cases and cumulative review of the world's literature.

BACKGROUND: The papillary cystic and solid tumor of the pancreas is rare. It occurs predominantly in young women, and most present a benign behavior. The pathogenesis of this tumor has attracted a number of investigations but remains unclear. METHODS: We present three patients with this tumor and a review of 289 others from the world's literature, a total of 292 cases. On the basis of the analyses of the clinical and pathologic features from the reported cases, the pathogenesis of this unusual tumor has been further explored. RESULTS: Ninety percent of the patients were female, with a mean age of 23.9 years. The tumors were usually quite large with a mean diameter of 10.3 cm. Ninety-two percent of these tumors were totally or partially cystic. Rupture of the capsule resulted in hemoperitoneum in eight cases, five of which were without any identifiable cause. Forty-three tumors (14.7%) have been recognized as malignant. The overall prognosis has been excellent and an aggressive approach to resection is indicated. CONCLUSIONS: The results of immunohistochemical staining and electromicroscopy were rather diverse, but most, including the current cases, support the hypothesis that the tumor originates from pleuripotential embryonic stem cells. Thus the term pancreatic embryonic tumors seems preferable to papillary cystic and solid tumor of the pancreas to delineate the origin of the tumor and to reflect some of its biologic characteristics.

Adolescent↗
PubMed1995

Carcinoma of the ampulla of Vater and mesenteric fibromatosis (desmoid tumor) associated with Gardner's syndrome: problems in management.

To date, 29 patients with Gardner's syndrome have been identified who developed carcinoma of the ampulla of Vater, and many others have been identified with mesenteric fibromatosis (desmoid tumor), but there have been only four cases of Gardner's syndrome with both ampullary carcinoma and mesenteric fibromatosis reported in the world literature. This article focuses on the complications and major problems in management resulting from the simultaneous occurrence of these two known features of Gardner's syndrome: carcinoma of the ampulla of Vater and fibromatosis (desmoid tumor) of the intestinal mesentery.

Adolescent↗
PubMed1995

Structure and specificity of T cell receptors expressed by potentially pathogenic anti-DNA autoantibody-inducing T cells in human lupus.

The production of potentially pathogenic anti-DNA autoantibodies in SLE is driven by special, autoimmune T helper (Th) cells. Herein, we sequenced the T cell receptor (TCR) alpha and beta chain genes expressed by 42 autoimmune Th lines from lupus patients that were mostly CD4+ and represented the strongest inducers of such autoantibodies. These autoimmune TCRs displayed a recurrent motif of highly charged residues in their CDR3 loops that were contributed by N-nucleotide additions and also positioned there by the recombination process. Furthermore, Th lines from four of the five patients showed a marked increase in the usage of the V alpha 8 gene family. Several independent Th lines expressed identical TCR alpha and/or beta chain sequences indicating again antigenic selection. 10 of these Th lines could be tested further for antigenic specificity. 4 of the 10 pathogenic anti-DNA autoantibody-inducing Th lines responded to the non-histone chromosomal protein HMG and two responded to nucleosomal histone proteins; all presented by HLA-DR molecules. Another Th line responded to purified DNA more than nucleosomes. Thus, these autoimmune Th cells of lupus patients respond to charged epitopes in various DNA-binding nucleoproteins that are probably processed and presented by the anti-DNA B cells they selectively help.

Amino Acid Sequence↗
PubMed1995

Interaction between intercalation type anticancer drugs and DNA studied by ultraviolet resonance Raman spectroscopy.

The interaction of typical intercalation type anticancer drugs, adriamycin (ADM) and aclacinomycin (ACM), with calf thymus DNA was studied first with ultraviolet resonance Raman spectroscopy (UVRRS). The results demonstrate that the important information such as intercalation sites of drugs, the electronic interaction and the hydrogen bonds between drugs and DNA can be obtained by UVRRS. The method can also show the influence of drugs on DNA conformation and hydrogen bonds between bases of DNA.

Aclarubicin↗
PubMed1995

Expression of p53 gene in oral squamous cell carcinoma and its relation with clinical and pathological parameters and prognosis of patients.

One hundred and eleven cases of oral squamous cell carcinoma (OSCC) were examined for overexpression of p53 protein by using immunohistochemical technique. Association between p53 protein overexpression and clinical and pathological parameters as well as prognosis of patients were also analyzed. p53 protein overexpression was commonly observed (69.4%) in OSCC and may be used as a marker of carcinogenesis of OSCC. The level of p53 protein overexpression is correlated with the lower three and five-year survival rate of OSCC. The presence or absence of p53 overexpression was not correlated with sex, age, site of tumor, size of tumor, degree of differentiation, node status, and clinical stage in OSCC. Single factor COX proportional hazards regression model analysis indicated that there was no significant association between p53 overexpression and prognosis of OSCC. Multivariable COX model analysis failed to establish effective life function or risk rate function. These showed that all the parameters analyzed in this study as well as p53 overexpression were not significant and effective risk factors of prognosis for patients with OSCC.

Carcinoma, Squamous Cell↗
PubMed1994

Two inverted repeats in the nodD promoter region are involved in nodD regulation in Rhizobium leguminosarum.

In Rhizobium leguminosarum (R.l.) biovar viciae, the nodulation gene nodD encodes a transcriptional activator (NodD) which binds to highly conserved DNA sequences (nod-boxes) in the promoters of other nod operons. In addition, NodD represses nodD transcription and this occurs at the divergent and overlapping nodA-nodD promoters. We mutagenised this region with hydroxylamine, and by cloning the mutagenised DNA into a vector carrying the lacZ reporter gene downstream from the cloning site identified mutations affecting nodD expression and repression. The resulting plasmids were transferred to R. l. viciae strains containing or lacking nodD. Two classes of promoter mutants were identified: those in which nodD transcription was altered and those in which NodD-dependent repression was altered. The nucleotide (nt) changes in the promoter region were found to be located within two inverted repeat sequences (A2 and A3) which are about 70 bp apart. A2 is important for nodD transcription and A3 (which is upstream from A2) is involved in NodD-dependent repression. The nt sequence at A3 shows some homology to the nod-box region of the nodA promoter. It is proposed that the NodD-dependent repression occurs as a result of NodD binding to both A3 and the nodA nod-box, forming a loop which prevents transcription of nodD from its promoter, A2, which lies between A3 and the nod-box. This model is supported by the observation that there are at least three sites for NodD binding in the nodA-nodD promoter region.

Bacterial Proteins↗
PubMed1994

T cell receptor alpha-chain repertoire of pathogenic autoantibody-inducing T cells in lupus mice.

The production of pathogenic anti-DNA autoantibodies in mice with lupus nephritis is dependent on special autoimmune Th cells that can also transfer the disease into preautoimmune mice. In previous work, these pathogenic Th cells were cloned and their TCR beta-chains were sequenced to reveal a recurrent motif of anionic residues in their CDR3 loops. Accordingly, approximately half of the Th clones were found to be specific for nucleosomal Ag that contain cationic residues. Herein, we analyzed the TCR alpha-chain repertoire of 15 of these pathogenic Th clones and found them to be heterogeneous, even among the nucleosome-specific Th clones. Most of these autoimmune TCR alpha-chains contained anionic residues in their CDR3 in addition to cationic residues. Therefore, these pathogenic Th clones of lupus probably recognize epitopes with mixed charge runs that are derived from autoantigens, such as histone-DNA complexes. Interestingly, the V alpha gene segments used by 10 of these Th clones derived from the (SWR x NZB)F1 lupus mice differed from previously reported sequences indicating that they were new members or alleles of the respective V alpha gene family. One of the Th clones used a gene from an entirely new murine V alpha gene family, identified here as V alpha 23, which consisted of approximately two members that were conserved among strains with different V alpha haplotypes. Knowledge of the primary structure of the TCR expressed by these pathogenic Th clones of lupus would help in the analysis of their antigenic specificities and also would be essential for studying their regulation in transgenic mice carrying these autoimmune TCR genes.

Amino Acid Sequence↗
PubMed1994

Cooperative DNA-protein interactions. Effects of changing the spacing between adjacent binding sites.

Cooperative binding of specific DNA-binding proteins plays crucial roles in gene regulatory circuitry, and is a model system for interactions between proteins bound to DNA. We have studied coliphage HK022 repressor, which binds to two adjacent operators with a cooperativity parameter of approximately 2000. We examined the effect of changing the spacing between these two operators on cooperativity and on the conformation of the complex. Maximum cooperativity was seen with the wild-type spacing; considerable cooperativity was retained for most spacing variants, but was abolished when the operators lay on opposite faces of the DNA helix. Most spacing variants conferred changes in the conformation of the DNA-protein complex. Our data indicate that the pairwise cooperativity observed with the wild-type spacing results from a conformation that prevents protein-protein contacts with flanking bound dimers. We conclude that protein-DNA complexes involving the same specific binding sites and the same protein molecules can adopt many different conformations, depending on the spacing between the binding sites. This conclusion may be broadly applicable to protein-DNA interactions in other systems.

Allosteric Regulation↗
PubMed1994

In vitro role of IL-1 in heightened IgG, anti-DNA, and nephritogenic idiotype production by B cells derived from the murine MRL/lpr lupus model.

The MRL/lpr murine model resembles human lupus both in its serologic and immunopathologic features, and is characterized by high-level IgG and autoantibody production. The precise mechanisms for this B cell hyperactivity are poorly understood. This study explored the role of IL-1 in determining high-level IgG and autoantibody production in the MRL/lpr murine lupus model by blocking IL-1 activity with a recombinant IL-1 receptor antagonist (IL-1Ra). IgG and autoantibody production (anti-DNA ab and Id-H130 activity) by B cells derived from MRL/lpr mice was significantly suppressed by treating B cell cultures with IL-1Ra. In contrast, IgG and autoantibody production by B cells derived from young MRL/lpr, MLR/++, or normal C3H/HeJ mice showed virtually no suppression with IL-1Ra. Collectively, these findings indicate that IL-1 may be an important factor in determining the heightened production of IgG, anti-DNA, and id-H130 antibody production in lupus-prone MRL/lpr mice. Furthermore, heightened IL-1 activity appears to be influenced by both age and the presence of the lpr mutation.

Animals↗
PubMed1994

Molecular analysis of G1B and G3A IFN gamma mutants reveals that defects in CIITA or RFX result in defective class II MHC and Ii gene induction.

Class II major histocompatibility complex (MHC) genes and the invariant (Ii) gene are inducible by interferon-gamma (IFN gamma) but not by interferon-alpha and interferon-beta. The promoter regions of these genes contain three regulatory elements that mediate constitutive and IFN gamma-induced expressions; however, none of the DNA-binding proteins that interact with these elements are regulated by IFN gamma. Recently, a gene coding for a transactivator (CIITA) of class II MHC genes that complements a HLA-DR-negative immunodeficiency has been isolated. Using one IFN gamma mutant cell line (G3A) that is selectively defective in HLA-DR and Ii induction, four lines of evidence are presented to show that CIITA mediates the IFN gamma induction of HLA-DR and Ii genes. Analysis of another mutant line, G1B, indicates that the lack of DRA and Ii gene induction by IFN gamma is correlated with the lack of RFX DNA binding activity, thus providing the link between RFX and an IFN gamma response.

Antigens, Differentiation, B-Lymphocyte↗