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PubMed1989

Interference by phosphatases in the spectrophotometric assay for phosphoenolpyruvate carboxylase.

The aim of this work was to discover the extent of interference by phosphoenolpyruvate (PEP) phosphatase in spectrophotometric assays of PEP carboxylase (EC 4.1.1.31) in crude extracts of plant organs. The presence of PEP phosphatase and lactate dehydrogenase (EC 1.1.1.27) in extracts leads to PEP-dependent NADH oxidation that is independent of PEP carboxylase activity, and hence to overestimation of PEP carboxylase activity. In extracts of three organs of pea (Pisum sativum L.: leaves, developing embryos, and Rhizobium nodules), two organs of wheat (Triticum aestivum L.: developing grain and endosperm), and leaves of Moricandia arvensis (L.) D.C., lactate dehydrogenase activity was at most only 16% of that of PEP carboxylase at the pH optimum for PEP carboxylase activity. Endogenous PEP phosphatase and lactate dehydrogenase are thus unlikely to interfere seriously with the assay for PEP carboxylase at its optimum pH. Addition of lactate dehydrogenase to PEP carboxylase assays- a proposed means of correcting for nonenzymic decarboxylation of oxaloacetate to pyruvate-resulted in increases in PEP-dependent NADH oxidation from zero (Rhizobium nodules) to 131% (wheat grains). There was no obvious relationship between the magnitude of this increase and conditions in the assay that might promote oxaloacetate decarboxylation. However, the magnitude of the increase was highly positively correlated with the activity of PEP phosphatase in the extract. Addition of lactate dehydrogenase to PEP carboxylase assays can thus result in very large overestimations of PEP carboxylase activity, and should only be used as a means of correction for oxaloacetate decarboxylation for extracts with negligible PEP phosphatase activity.

Journal Article↗
PubMed2005

Natural resistance-associated macrophage protein 1 gene polymorphisms in rheumatoid arthritis.

OBJECTIVES: To investigate the association of natural resistance-associated macrophage protein 1 gene (NRAMP1) polymorphisms with rheumatoid arthritis (RA) in Taiwan. METHODS: NRAMP1 polymorphisms were determined from 113 RA patients and 74 healthy controls using the polymerase chain reaction/restriction fragment length polymorphism method. RESULTS: The genotype frequencies of NRAMP1 823 C/C, 1703G/G (543D/D), and 1729+55 del 4 TGTG+/+ (244/244) were significantly higher in patients with RA than in controls. Similar findings were also evident in allele frequencies and allele carriage frequencies of 823C, 1703G (543D), and 1729+55 del 4 TGTG+ (244). The associations of these polymorphisms with RA were independent of HLA-DR4. Linkage disequilibria could be found between 823C and 1703G, and between 1703G and 1729+55 del 4 TGTG+. The estimated haplotype frequency of NRAMP1 823C/1703G/1729+55 del 4 TGTG+ was significantly increased in RA patients compared with controls. We also found that patients with 823 C/C had a significantly lower prevalence of rheumatoid nodule than those without 823 C/C. CONCLUSION: NRAMP1 823C, 1703G (543D), and 1729+55 del 4 TGTG+ (244) are precipitating factors for the development of RA in Taiwan. The estimated NRAMP1 823C/1703G/1729+del 4 TGTG+ haplotype is associated with susceptibility to RA. NRAMP1 823 C/C prevents the development of rheumatoid nodule in RA patients.

Alleles↗
PubMedDate not supplied

Changing trends in thyroid practice: understanding nodular thyroid disease.

OBJECTIVE: To describe changes that have occurred between 1952 and 2002 in the evaluation and management of nodular thyroid disease. METHODS: A 30-year personal experience, institutional contributions, and the related published literature on evaluation of thyroid function and evolving strategies for management of thyroid nodules are reviewed. RESULTS: Triiodothyronine (T(3)) was discovered in 1952, and measurement of plasma thyroxine by a competitive protein-binding technique became available in the 1960s. Late during that decade, the first radioimmunoassay for thyroid-stimulating hormone (TSH) was described, modified, and then used in clinical practice until the mid-1980s, when the more sensitive TSH assays became widely available. T(3) determination by radioimmunoassay was introduced early in the 1970s. Currently, sensitive thyroid function tests can detect early disease. In the general population, thyroid nodules have a prevalence higher than 50% after age 65 years, affecting more than 100 million people in the United States. Two important developments influenced thyroid nodule evaluation and management-- fine-needle aspiration (FNA) biopsy and ultrasonography. Because FNA biopsy has emerged as the most accurate test for nodule diagnosis, it has decreased the need for scanning and for thyroidectomy and thereby is likely to reduce health-care costs by more than $500 million annually in the United States. Thyroid ultrasonography is the imaging method of choice for evaluation of thyroid gland structure. Management of cytologically benign thyroid nodules remains controversial. CONCLUSION: TSH seems to be only one of many factors in pathologic thyroid growth. FNA, because of its diagnostic accuracy, should be the initial procedure used in nodule evaluation.

Antithyroid Agents↗
PubMed2005

Targeting toll-like receptor 9 with CpG oligodeoxynucleotides enhances tumor response to fractionated radiotherapy.

Synthetic oligodeoxynucleotides containing unmethylated CpG motifs detected by Toll-like receptor 9 of dendritic cells and B cells have potent immunomodulatory effects. CpG oligodeoxynucleotides induce cytokines, activate natural killer cells, and elicit T-cell responses leading to antitumor effects, including improved efficacy of chemotherapeutic agents and, as we reported recently, synergy between CpG oligodeoxynucleotide 1826 and single-dose radiotherapy of an immunogenic mouse fibrosarcoma. The present study extends this finding to the fractionated radiotherapy of the fibrosarcoma tumor and assesses the ability of CpG oligodeoxynucleotide 1826 to increase the radioresponse of a tumor (nonimmunogenic fibrosarcoma). The experiments used a murine immunogenic fibrosarcoma tumor, fibrosarcoma growing in the leg of mice, and response to radiotherapy was assessed by tumor growth delay and tumor cure rate (TCD50, radiation dose yielding 50% tumor cure). Multiple s.c. peritumoral or i.t. administrations of CpG oligodeoxynucleotide 1826 at a dose of 100 microg per mouse were given when established tumors were 6 mm in diameter. Local tumor irradiation was initiated when tumors grew to 8 mm in diameter; radiation was delivered in 1 to 9 Gy fractions given twice daily separated by 6 to 7 hours for 5 consecutive days to achieve a total dose of 10 to 90 Gy. CpG oligodeoxynucleotide 1826, given as a single agent, had only a small antitumor effect, but it dramatically enhanced fibrosarcoma response to radiotherapy. Although 83.1 (79.2-90.0) Gy total dose were needed to achieve tumor cures in 50% of mice treated with radiotherapy alone, only 23.0 (11.5-32.7) Gy total dose were needed in mice treated with both CpG oligodeoxynucleotide 1826 and radiotherapy. The magnitude of potentiation of tumor radioresponse at the TCD50 level was by a factor of 3.61, a much higher value than that (a factor of 1.93) that we reported for single-dose radiotherapy. Mice cured of their tumors by combined CpG oligodeoxynucleotide 1826 plus radiotherapy were highly resistant to s.c. tumor take or development of tumor nodules in the lung from i.v. injected tumor cells when rechallenged with fibrosarcoma cells 100 to 120 days after the treatment, suggesting the development of a memory response. CpG oligodeoxynucleotide 1826 also increased radioresponse of the nonimmunogenic fibrosarcoma tumor by a factor of 1.41 and 1.73 when CpG oligodeoxynucleotide 1826 was given s.c. and i.t., respectively. These findings show that CpG oligodeoxynucleotides are highly potent enhancers of tumor response to both single-dose and fractionated radiation and as such have potential to improve clinical radiotherapy.

Animals↗
PubMed1989

Offset electrocardiographic electrode simulating a pulmonary nodule on radiographs.

A recently developed type of electrocardiographic (ECG) monitoring electrode may simulate a pulmonary nodule on chest radiographs. The artifact results from the offset design of the electrode, which contrasts with the configuration of conventional electrodes. Awareness of this potential artifact is important to prevent misdiagnosis.

Diagnostic Errors↗
PubMed1999

Detection of sarcolectin-specific receptors like the cytokine macrophage migration inhibitory factor in rheumatoid nodules.

The objective of this study was the evaluation of the relation between the N-acetyl-neuraminic acid-binding endogenous lectin sarcolectin and the cytokine macrophage migration inhibitory factor (MIF) during development of rheumatoid nodules (RN) in seropositive rheumatoid arthritis (RA). Sarcolectin was purified and biotinylated. The binding patterns of this probe were analyzed in RN from patients with RA (n = 23) and compared with the distribution of antibodies with specificity for MIF, fibrin, fibronectin. In early RN, all areas of the inflammatory tissue displayed presence of receptors for sarcolectin. Macrophages were especially positive. In mature rheumatoid nodules binding of sarcolectin was restricted to the periphery of necrotic areas, to endothelial cells and perivascular connective tissue of marginal zones. Distribution patterns of MIF were similar but not identical. The histological staining characteristics demonstrate sarcolectin-binding receptors in RN that are altered upon disease progression. The finding suggests that specific interactions between this endogenous lectin and MIF may be involved in the course of RA.

Adult↗
PubMed2000

Aluminium-induced granulomas after inaccurate intradermal hyposensitization injections of aluminium-adsorbed depot preparations.

BACKGROUND: The development of persistent subcutaneous nodules at the injection sites of aluminium-adsorbed hyposensitization solutions is rare. These nodules have been interpreted as a delayed, granulomatous hypersensitivity reaction to aluminium. We report for the first time a case of persistent intradermal granulomas that developed at the sites of inaccurate intradermal, instead of subcutaneous, hyposensitization injections. METHODS: An intradermal nodule was excised and processed for histopathology, scanning electron microscopy, and X-ray microanalysis. Intradermal and patch tests with aluminium hydroxide were performed. RESULTS: Histologically, the nodule presented a pattern of granulomatous inflammatory reaction surrounding foci of necrotic tissue. Scanning electron microscopy and X-ray microanalysis revealed deposits of aluminium within the granulomas. Patch tests with aluminium hydroxide were negative, and intradermal tests caused persistent intradermal granulomas. Subsequent hyposensitization therapy in our department with the usual subcutaneous injections of aluminium-adsorbed allergen extracts was well tolerated by the patient. CONCLUSIONS: Local toxic effects of aluminium may be crucial in the development of persistent intradermal injection-site granulomas. Such intradermal nodules may develop even if the subcutaneous route is well tolerated. We conclude that inaccurate intradermal injections of aluminium-containing solutions have to be strictly avoided.

Aluminum Hydroxide↗
PubMed1998

Epibulbar allergic granulomatous nodules in a human immunodeficiency virus-positive patient.

PURPOSE: To report an unusual epibulbar inflammatory process in a patient with human immunodeficiency virus (HIV). METHODS: Case report. A 32-year-old man developed fleshy epibulbar nodules on his right conjunctiva and cornea after being treated for conjunctivitis. A biopsy of the lesions was done, and the specimen was processed for histopathologic examination. RESULTS: The biopsy specimen contained inflammatory cells, including an eosinophilic abscess. The diagnosis was allergic granulomatous nodules. CONCLUSION: This case illustrates the occurrence of epibulbar allergic granulomatous nodules in an HIV-positive patient.

Adult↗
PubMed1992

Subcutaneous nodules as the first clinical manifestation of sarcoidosis.

We report the case of a 61-year-old male who presented with a febrile illness accompanied by arthralgia and myalgia. Two months later he developed multiple subcutaneous nodules and enlarged parotid glands. Later two erythematous plaques, clinically compatible with erythema nodosum (EN), were observed. Laboratory investigations revealed abnormal levels of angiotensin converting enzyme and chest radiography showed bilateral hilar enlargement. The biopsy of the cutaneous lesions demonstrated multiple non-caseating granulomas in the subcutaneous tissue without any alterations in the epidermis and the dermis. The cultures for Mycobacteria and fungi were both negative. The clinical picture and histopathological findings were compatible with subcutaneous nodular sarcoidosis. The response to steroid treatment was satisfactory.

Connective Tissue↗
PubMed1995

Chemoprevention by S-adenosyl-L-methionine of rat liver carcinogenesis initiated by 1,2-dimethylhydrazine and promoted by orotic acid.

Chemoprevention of liver carcinogenesis by S-adenosyl-L-methionine (SAM) was studied in F344 male rats. The rats were given 1,2-dimethylhydrazine (1,2-DMH) 2 HCl (100 mg/kg, i.p.) 18 h after two-thirds hepatectomy. One week later they were fed a semisynthetic basal diet containing 1% orotic acid (OA) for 29 weeks. At this time the rats were transferred to the basal semisynthetic diet and were killed 3 weeks later. SAM treatment (384 mumol/kg/day, i.m.), was started 1 week after 1,2-DMH and was continued up to the end of the experiment. Controls received solvent alone. SAM exerted an inhibitory effect on the induction of preneoplastic and neoplastic lesions. For example, nodules with diameters of 1-2 and 2-6 mm exhibited a decrease in both incidence and number per liver, while no such inhibitory effect was seen in the category of larger nodules. Furthermore, hepatocellular carcinoma (HCC) also exhibited a decrease in the SAM-treated group. The number/liver and incidence were 0.04 and 4.8% respectively in the SAM-treated group, compared to 0.38 and 37.8% in the control group. Microscopic examination showed the presence of well-differentiated carcinomas and atypical nodules in control rats, while only one small, well-differentiated tumor and one nodule with patterns of initial transformation were seen in SAM-treated rats. No patchy staining of glutathione-S-transferase, indicative of remodeling, was observed in nodules of both SAM-treated and control rats. Nodules and HCCs developing in SAM-treated rats exhibited a relatively high number of apoptotic bodies. Apoptotic bodies count showed 2.8- and 1.8-fold increases in nodules and HCCs of SAM-treated rats with respect to controls. These results indicate that SAM exerts a chemopreventive effect on hepatocarcinogenesis induced by the OA model. SAM seems to be more effective in inhibiting nodule to HCC progression than on the growth of nodule per se. The inhibitory effect is associated with an increase in cell loss by apoptosis in nodules and HCC.

1,2-Dimethylhydrazine↗
PubMed1997

Induced drug resistance inhibits selection of initiated cells and cancer development.

Compounds exerting a mitoinhibitory effect on normal hepatocytes are potent promoters in the resistant hepatocyte model of chemical carcinogenesis in combination with stimulation of regenerative growth by partial hepatectomy or treatment with carbon tetrachloride. 2-Acetylaminofluorene (2-AAF) almost completely inhibits liver cell regeneration after partial hepatectomy, allowing only resistant cells to participate in regenerative growth. After initiation by diethylnitrosamine and promotion with 2-AAF and partial hepatectomy (PH), focal growth of initiated cells generates liver lesions which occupy 40% of the hepatic volume three weeks after PH. In this work the mechanism for the anti promoting effects of phenobarbital and 3-methylcholantrene were investigated as well as their effects on the development of malignant hepatocellular carcinoma in the resistant hepatocyte model. Treatment with phenobarbital or, especially, 3-methylcholanthrene rendered normal rat hepatocytes resistant to the mitoinhibitory effect of 2-AAF. In combination with 2-AAF/PH, 3-methylcholanthrene shortened the regenerative growth period to less than one week. In the Solt-Farber protocol for experimental hepatocarcinogenesis, treatment with phenobarbital or 3-methylcholanthrene during promotion with 2-AAF/PH permitted hepatocytes surrounding the focal lesions to respond with regenerative growth. The foci and surrounding liver grew until the liver/body mass index reached the control value. With phenobarbital treatment the total focal volume was 20% of the liver volume three weeks after PH, whereas the corresponding value in the case of 3-methylcholanthrene was only 1%. Labelling index data supported the conclusion that growth of the liver lesions in the resistant hepatocyte model was dependent on differential inhibition of normal hepatocyte growth by the promoter and that the size of the foci obtained was related to the length of time after PH required to complete liver regeneration. 3-methylcholanthrene induced 2-AAF resistance prevented the development of large persistent nodules and hepatocellular carcinoma while phenobarbital delayed cancer development with several month. The data thus supports the idea that the degree of clonal expansion during promotion determines the size of the population at risk for malignant transformation, as well as the final frequency of carcinomas.

2-Acetylaminofluorene↗
PubMed1976

Cytology and cytogenesis of neoplastic (hyperplastic) hepatic nodules.

Cytochemical and electron microscopic investigations of neoplastic nodules induced in the rat liver by nitrosomorpholine or thioacetamide show that most neoplastic nodules are comprised of a rather heterogeneous cell population. At least four different types of altered hepatocytes can be distinguished: (a) "clear" glycogen storage cells with a dislocation and relative reduction of the granular endoplasmic reticulum; (b) "acidophilic" glycogen storage cells with a hypertrophy of the agranular endoplasmic reticulum; (c) fat-storing cells; and (d) basophilic cells poor in glycogen and rich in ribosomes. In addition, there are diverse intermediate cell types. The cytochemically demonstrable activity of glucose-6-phosphatase is reduced in most neoplastic nodules, but it may also be normal or even increased. The clear and the acidophilic cells precede the development of the neoplastic nodules by weeks and months. They usually form foci which are taken to be preneoplastic lesions. During the formation of neoplastic nodules and hepatocellular carcinomas originating for such foci the glycogen of the clear and the acidophilic cells is progressively reduced, whereas the number of ribosomes (basophilia) increases. This process, which may be accompanied by a transitory accumulation of fat, leads to the evolution of basophilic carcinoma cells. We conclude from these observations that the majority of the neoplastic nodules consist of a mixture of precancerous, definitely cancerous, and diverse intermediate cells. Neoplastic nodules in which basophilic cells prevail may already be carcinomas. Although the neoplastic nodules seem to be a frequent precursor of hepatocellular carcinomas, the latter may also develop without going through the nodule stage.

Animals↗
PubMed2006

The sources of parenchymal regeneration after chronic hepatocellular liver injury in mice.

After liver injury, parenchymal regeneration occurs through hepatocyte replication. However, during regenerative stress, oval cells (OCs) and small hepatocyte like progenitor cells (SHPCs) contribute to the process. We systematically studied the intra-hepatic and extra-hepatic sources of liver cell replacement in the hepatitis B surface antigen (HBsAg-tg) mouse model of chronic liver injury. Female HBsAg-tg mice received a bone marrow (BM) transplant from male HBsAg-negative mice, and half of these animals received retrorsine to block indigenous hepatocyte proliferation. Livers were examined 3 and 6 months post-BM transplantation for evidence of BM-derived hepatocytes, OCs, and SHPCs. In animals that did not receive retrorsine, parenchymal regeneration occurred through hepatocyte replication, and the BM very rarely contributed to hepatocyte regeneration. In mice receiving retrorsine, 4.8% of hepatocytes were Y chromosome positive at 3 months, but this was frequently attributable to cell fusion between indigenous hepatocytes and donor BM, and their frequency decreased to 1.6% by 6 months, as florid OC reactions and nodules of SHPCs developed. By analyzing serial sections and reconstructing a 3-dimensional map, continuous streams of OCs could be seen that surrounded and entered deep into the nodules of SHPCs, connecting directly with SHPCs, suggesting a conversion of OCs into SHPCs. In conclusion, during regenerative stress, the contribution to parenchymal regeneration from the BM is minor and frequently attributable to cell fusion. OCs and SHPCs are of intrinsic hepatic origin, and OCs can form SHPC nodules.

Animals↗
PubMed2005

Sarcoidosis occurring after interferon-alpha therapy for chronic hepatitis C: report of two cases.

We report two patients who were diagnosed with sarcoidosis after receiving interferon (IFN)-alpha therapy for chronic hepatitis C, and conduct a review the relevant literature. The first patient was a 52-year-old female who developed multiple subcutaneous nodules 2 months after finishing IFN-alpha therapy. A skin biopsy from subcutaneous nodules on the right elbow joint revealed sarcoid granulomata. These lesions resolved spontaneously 4 months later. The second patient, a 57-year-old male, developed bilateral hilar and mediastinal lymph node enlargement 2 years after finishing IFN-alpha 2a therapy. A transbronchial lung biopsy demonstrated sarcoid granulomata. In addition, he had uveitis and left ulnar nerve involvement. His eye and nerve involvement gradually improved over 20 months. It is feasible that IFN therapy has been a trigger for sarcoidosis in these patients.

Antiviral Agents↗
PubMed2004

Metastasis-associated protein 1 deregulation causes inappropriate mammary gland development and tumorigenesis.

Emerging data suggest that metastasis-associated protein 1 (MTA1) represses ligand-dependent transactivation functions of estrogen receptor-alpha in cultured breast cancer cells and that MTA1 is upregulated in human breast tumors. However, the role of MTA1 in tumorigenesis in a physiologically relevant animal system remains unknown. To reveal the role of MTA1 in mammary gland development, transgenic mice expressing MTA1 under the control of the mouse mammary tumor virus promoter long terminal repeat were generated. Unexpectedly, we found that mammary glands of these virgin transgenic mice exhibited extensive side branching and precocious differentiation because of increased proliferation of ductal and alveolar epithelial cells. Mammary glands of virgin transgenic mice resemble those from wild-type mice in mid-pregnancy and inappropriately express beta-casein, cyclin D1 and beta-catenin protein. Increased ductal growth was also observed in the glands of ovariectomized female mice, as well as of transgenic male mice. MTA1 dysregulation in mammary epithelium and cancer cells triggered downregulation of the progesterone receptor-B isoform and upregulation of the progesterone receptor-A isoform, resulting in an imbalance in the native ratio of progesterone receptor A and B isoforms. MTA1 transgene also increased the expression of progesterone receptor-A target genes Bcl-XL (Bcl2l1) and cyclin D1 in mammary gland of virgin mice, and, subsequently, produced a delayed involution. Remarkably, 30% of MTA1 transgenic females developed focal hyperplastic nodules, and about 7% exhibited mammary tumors within 18 months. These studies establish, for the first time, a potential role of MTA1 in mammary gland development and tumorigenesis. The underlying mechanism involves the upregulation of progesterone receptor A and its targets, Bcl-XL and cyclin D1.

Animals↗
PubMed1994

Computerized detection of pulmonary nodules in computed tomography images.

RATIONALE AND OBJECTIVES: Interpretation of computed tomographic (CT) scans of the lungs is a time-consuming task that involves visual correlation of possible nodules in one section with those in contiguous sections to distinguish actual nodules from blood vessels. Thus, the authors are developing automated methods to detect nodules on CT images of the thorax. METHODS: The computerized technique uses various computer-vision techniques and a priori information of the morphologic characteristics of pulmonary nodules. In each section, the external thoracic wall and lung boundaries are detected, and the features within the lung boundaries are subjected to gray-level thresholding operations. By analyzing the relationships between features arising at different threshold levels with respect to their shape, size, and location, each feature is assigned a likelihood of being a nodule or a vessel. Features in adjacent sections are compared to resolve ambiguous features. Detected nodule candidates are displayed in three dimensions within the lung. RESULTS: The system provided a sensitivity of 94% for nodule detection and an average of 1.25 false-positive results per case. CONCLUSIONS: Continued development of an automated method for detecting pulmonary nodules in CT scans is expected to aid radiologists in the task of locating nodules in three dimensions.

Artificial Intelligence↗
PubMed1989

Subcutaneous nodules in rheumatic fever.

Acute rheumatic fever is described in a six year old Ethiopian male child who first presented with subcutaneous nodules and later developed carditis.

Acute Disease↗
PubMed2004

Inhibition of liver carcinogenesis in Wistar rats by consumption of an aqueous extract from leaves of Ardisia compressa.

This study evaluates the chemopreventive effect of an aqueous extract of dried leaves of Ardisia compressa against liver cancer. A rat liver assay that mimics progressive forms of human disease was used as a carcinogenesis model. Forty-five male Wistar rats (180-200 g body weight) were injected intraperitoneally on day 1 with a single dose (100 mg/kg) of diethylnitrosamine (DEN), and also received via gavage 20 mg/kg acetylaminofluorene (2-AAF), on days 7, 8 and 9. The rats were randomly divided into four groups (n=15). Control groups (Group 1 and Group 2) had free access to water. Group 3 received 0.5% (w/v) of A. compressa tea for 10 days before treatment and during the study as the sole source of fluid until the rats were killed. A fourth group of 15 rats received no carcinogen or promoter but did receive 0.5%, (w/v) of A. compressa tea. All animals had 70% partial hepatectomy at day 10. The incidences of hepatocellular foci, nodules and carcinoma were significantly smaller in Group 3 than in Group 2 (P<0.01). A. compressa tea consumption alone (Group 4) did not induce the development of foci, nodules or carcinomas (P<0.01). The striking observation of this study was that consumption of A. compressa tea resulted in complete inhibition of the chemically-induced hepatocarcinogenesis in Wistar rats.

2-Acetylaminofluorene↗