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PubMed1986

Effect of glutathione and N-acetylcysteine on hepatocellular modifications induced by 2-acetylaminofluorene.

The exposure of rats to a dietary regimen containing 2-acetylaminofluorene induces a sequence of hepatocellular alterations leading to the development of preneoplastic nodules. Groups of 2-acetylaminofluorene-treated rats were given glutathione or N-acetylcysteine to evaluate the effects of these different thiols on the sequence of events that originate transformed cells. It is well known that intracellular thiols protect biological macromolecules from scavenging free radicals and electrophilic compounds produced by the metabolism of chemical agents. Male Wistar rats were maintained on a feeding regimen containing 0.05% 2-acetylaminofluorene. The diet of 2 groups of 2-acetylaminofluorene-treated animals was supplemented with either 0.1% glutathione or N-acetylcysteine. The effects in the liver of the exogenously supplied thiols during 2-acetylaminofluorene treatment were assessed evaluating DNA damage, glutathione levels, activity of marker enzymes glucose-6-phosphatase, gamma-glutamyltranspeptidase, and glutathione-S-transferase, survival rates, and development of salivary gland tumors. Our results demonstrate that the mortality due to 2-acetylaminofluorene exposure was reduced or completely abolished by thiols and that the development of salivary gland tumors was inhibited. Exogenously supplied thiols significantly reduced DNA damage as assessed by alkaline elution. At the doses employed, glutathione and N-acetylcysteine induce early stimulation of glutathione-S-transferase, had little effect on the loss of glucose-6-phosphatase activity and scanty influence on the net increase in gamma-glutamyltranspeptidase activity.

2-Acetylaminofluorene↗
PubMedDate not supplied

Traumatic keratoacanthoma arising in a 15-year-old boy following a motor vehicle accident.

Keratoacanthomas appear most commonly in sun-damaged skin in middle-aged and elderly people. We present a 15-year-old boy who developed a rapidly growing nodule within a hypertrophic scar that was the result of trauma suffered in a roll-over motor vehicle accident 8 months prior to presentation. Histologic analysis of a biopsy specimen of the nodule confirmed the presence of squamous cell carcinoma, keratoacanthoma type. The development of keratoacanthoma has been associated with sun exposure, chemical carcinogens, radiation therapy, genetic factors, and various forms of antecedent trauma, including surgery or grafting, thermal burns, laser resurfacing, and vaccination. This report describes the youngest patient with traumatically-induced keratoacanthoma, and is the first instance of this entity arising in a friction burn.

Accidents, Traffic↗
PubMed1999

Early events of hepatic metastasis formation in mice: role of Kupffer and NK-cells in natural and interferon-gamma-stimulated defense.

Surgical manipulation of a tumor may result in increased influx of tumor cells into the systemic and portal circulation and give rise to formation of metastases. In addition, major surgery has been reported to cause profound immunosuppression. In an attempt to increase the host-antitumor immune mechanisms following surgery we have studied the effect of preoperative administration of interferon-gamma, related to the antimetastatic effects of Kupffer cells (KC) and natural killer cells (NK-cells) in the early phase of liver metastasis formation. Colon carcinoma cells were injected into the superior mesenteric vein of syngeneic mice and after 17 days metastases were quantified by weight, number, and uptake of [125I]iododeoxyuridine. Unstimulated control mice developed 10.5 surface nodules per liver 17 days following injection of colon carcinoma cells into the superior mesenteric vein of syngeneic mice. This figure was only 2.6 in mice stimulated with a single dose of 1000 IU IFN-gamma 4 h prior to inoculation of tumor cells. Administration of GdCl3, which is reported to deplete and block the function of Kupffer cells, 24 h prior to tumor cell inoculation resulted in a 5-fold tumor mass increase relative to control. Injection of anti-asiolo-GM1 antiserum, which eliminates the hepatic NK-cells, induced a 10-fold increase in tumor mass. These results indicate an important early antimetastatic function of hepatic NK-cells and KC and that presurgical administration of IFN-gamma may be important for eliminating circulating tumor cells and inhibiting development of residual tumors.

Animals↗
PubMed2000

Supraglottic activity: evidence of vocal hyperfunction or laryngeal articulation?

False vocal fold (FVF) adduction and compression of the arytenoid cartilages to the petiole of the epiglottis in an anterior to posterior (A-P) direction have been thought to characterize voice disorders with abnormally increased muscle tension or effort, often termed hyperfunctional voice disorders. To further evaluate the association between hyperfunctional voice disorders and supraglottic activity, we compared the incidence of static and dynamic supraglottic activity in individuals with normal laryngeal mucosa, normal voice quality, and no voice complaints to two populations: subjects with vocal fold nodules and subjects with complaints of dysphonia without visible vocal fold lesions, glottal incompetence, or impairment of arytenoid cartilage motion ("hyperfunctional" group). Thirty-two subjects were assigned to one of these three groups (10 control, 12 nodule, and 10 hyperfunctional). Laryngeal movements were recorded using flexible videoendoscopy while a subject was performing speech tasks such as sustained phonation, syllable repetitions, sentence imitations, and conversation. Samples were randomized by subject and task and rated for presence or absence of A-P and FVF compression. Statistically significant group differences were found for FVF compression across speech tasks (chi-square, p<0.001). The control group had the smallest incidence (45%), nodule patients the next larger incidence (68%), and hyperfunctional patients the largest incidence (80%). Statistically significant group differences were found for A-P compression across speech tasks (chi-square, p<.05). The control group had the smallest incidence (74%), nodule patients the next larger incidence (78%), and hyperfunctional patients the largest incidence (92%). Statistically significant task differences were found for the presence of FVF compression in control subjects (chi-square, p<.005), hyperfunctional patients (chi-square, p<.025), and nodule patients (chi-square, p<.001), but not for A-P compression for any of the groups. A higher incidence of FVF compression was present for the speech tasks that included glottal stops. This context-specific variation in supraglottic activity suggested a dynamic component to FVF compression and also explained the high proportion of FVF compression in the control group. Each video sample was also rated for consistency of FVF or A-P compression to explore the static and dynamic nature of supraglottic activity. For samples on which raters agreed, A-P compression was typically present consistently, suggesting a static component, and FVF compression inconsistently, suggesting a dynamic component, for all three groups (chi-square, p<.001). These findings do not support previous suggestions that supraglottic activity may be a precursor to developing vocal fold nodules, as the nodule patients did not exhibit a higher incidence or consistency of A-P or FVF compression than patients with hyperfunctional voicing patterns in this study. Subjects in the hyperfunctional voice group were found to have static components of FVF and A-P compression. The presence of FVF compression in speech tasks that included glottal stops in the control group suggests an articulatory function at the laryngeal level.

Adolescent↗
PubMedDate not supplied

Studies on the antitumor activities of pyrimidinone-interferon inducers. Part 2. Potentiation of antitumor resistance mechanisms.

In continuation of studies on antitumor activities of pyrimidinone interferon inducers, we report here that 2-amino-5-bromo-6-mF-phenyl-4(3H)-pyrimidinone (ABmFPP) is similarly effective to 2-amino-5-bromo-6-phenyl-4-pyrimidinone (ABPP) in its ability to reduce the number of metastatic nodules of a spontaneous fibrosarcoma (NFSa) and a spontaneous mammary carcinoma (MCa-K) in the lungs of C3Hf/Kam mice. Both compounds were more effective when given to mice prior to, rather than after, intravenous transplantation of tumor cells. In studies on the mechanism of the antitumor activity of pyrimidinones, 2-amino-5-iodo-6-phenyl-4-pyrimidinone (AIPP) was used in addition to ABPP and ABmFPP. These agents were capable of activating peritoneal macrophages that thus became capable of lysing in vitro 3T12 transformed cells but not syngeneic BALB/c embryo fibroblasts. Also, these agents were capable of augmenting significantly the natural killer (NK) cell activity in the spleen of C3Hf/Kam mice. Spleen cells from treated mice admixed to NFSa cells inhibited in vivo tumor take of these cells when the admixture was injected subcutaneously. Pyrimidinones were also effective against the development of NFSa nodules in the lungs of T-cell deficient mice implying that the presence of T-cells is not a prerequisite for the induction of antitumor activity by these agents. A further observation was that pyrimidinone compounds reduced the metastasis formation enhancing effect of cyclophosphamide. Therefore, pyrimidinone interferon inducers exhibit an appreciable antimetastatic activity mediated through antitumor resistance mechanisms involving activation of macrophages and stimulation of NK-cells.

Animals↗
PubMed1999

Expression of TGF-beta isoforms and their receptors during mineralized nodule formation by rat periodontal ligament cells in vitro.

Transforming growth factor-betas (TGF-beta s) and bone morphogenetic proteins (BMPs), members of a TGF-beta superfamily, are known to play an important role in osteogenic cell differentiation and consequently bone formation. We have reported previously that periodontal ligament (PDL) cells differentiate and form mineralized nodules when cultured in the presence of dexamethasone (Dex), beta-glycerophosphate (GP) and ascorbic acid (AA). To understand the roles of TGF-beta isoforms (TGF-beta 1, 2 and 3) and TGF-beta type I receptors (activin receptor-like kinase (ALK)-2, -3, -5 and -6) in PDL cell differentiation, their expression was investigated using Northern blot analysis. Rat PDL cells, derived from coagulum in the tooth socket, were cultured in the presence of Dex (5 microM), GP (10 mM) and AA (50 micrograms/ml) for up to 21 d. Total RNA was isolated from PDL cells after 0, 7, 14 and 21 d and used for northern blot analysis of mRNAs for matrix proteins, TGF-beta isoforms and their receptors using 32P-labeled cDNAs as probes. Four stages showing distinct morphological characteristics and matrix expression during development of mineralized nodules were identified. Type I collagen (Col I) and SPARC (secreted protein, acidic and rich in cysteine) mRNAs were expressed at the confluent stage, but decreased during the mineralization stage. Osteopontin (OPN) and alkaline phosphatase (ALP) transcripts were initially observed at multilayer stage, while bone sialoprotein (BSP) and osteocalcin (OC) at the nodule stage and all 4 were expressed thereafter. TGF-beta 1 mRNA expression increased with the progression of PDL cell differentiation, while a relatively high level of TGF-beta 3 transcript decreased slightly during their differentiation. TGF-beta 2 mRNA was not expressed. The expression of TGF beta-RI mRNA decreased, whereas that of TGF beta-RIII increased dramatically with PDL cell differentiation. TGF beta-RII gene activities remained high throughout all stages. ALK-2, ALK-3 and ALK-6 mRNA expression increased with the progression of PDL cell differentiation, suggesting that these receptors may play important roles in Dex-induced PDL cell differentiation and mineralized nodule formation.

Animals↗
PubMed1996

A new hepadnavirus endemic in arctic ground squirrels in Alaska.

We present evidence for a novel member of the hepadnavirus family that is endemic in wild arctic ground squirrels (Spermophylus parryi kennicotti) in Alaska. This virus, designated arctic squirrel hepatitis virus (ASHV), was initially detected in the livers of animals bearing large hepatic nodules by nucleic acid hybridization with hepadnavirus probes and in plasma by cross-reactivity with antibodies to hepadnavirus surface and core antigens. The complete nucleotide sequence of the 3,302-bp-long ASHV genome was determined and compared with those of ground squirrel hepatitis virus (GSHV) and woodchuck hepatitis virus (WHV); all sequences were organized into four open reading frames, designated pre-C/C, pre-S/S, pol, and X. Despite roughly equivalent variability among the three rodent hepadnaviruses (around 16% base and 19% amino acid exchanges), ASHV appeared to be more closely related to GSHV than to WHV in phylogenetic analysis. Accordingly, preliminary studies of the pathology of ASHV infection suggested that ASHV may be a less efficient oncogenic agent than WHV. About one-third of aged animals maintained in captivity, including virus-infected as well as uninfected squirrels, developed large liver nodules, consisting of hepatocellular adenomas or carcinomas or nonmalignant lesions characterized by drastic microvesicular steatosis. ASHV-infected arctic ground squirrels may serve as a new model with which to analyze the contribution of hepadnavirus- and host-specific determinants to liver pathology and tumorigenesis.

Alaska↗
PubMed1987

Invasiveness, metastasis, and transplantability of mouse liver nodules.

Data are presented which show that various mouse liver nodular lesions, such as hyperplastic nodules, hepatocellular adenomas, and hepatocellular carcinomas, differ not only morphologically but also biologically regarding their behavior in the primary and secondary hosts. The hyperplastic nodules grew slowly by expansion without affecting the integrity of the lobular structure. The primary hepatocellular adenomas also grew slowly by expansion but eliminated the histoid liver structure. Neither lesions metastasized to the regional lymph nodes and distant organs. Upon isogeneic transplantation, the adenomas required a long latent period before manifesting an expansive type of growth without invasion and metastasis. The primary hepatocellular carcinomas grew fast, destroyed surrounding parenchyma, and those showing moderately to poorly differentiated cellular morphology metastasized to regional lymph nodes and distant organs. Upon transplantation hepatocellular carcinomas grew fast, invaded locally, metastasized distantly, and killed the recipients within a few weeks. Thus hepatocellular adenomas and carcinomas represent two distinct entities both morphologically and biologically. Thus the agents should be classified according to the type of nodular liver lesions they "induce" in the mouse liver. The least innocuous agents would be those resulting in the development of hyperplastic nodules. They should not be labelled as hepatocarcinogens. On the other side of the spectrum should be the agents "inducing" the hepatocellular carcinomas and they should be classified as mouse liver carcinogens. The agents capable of affecting significantly the hepatocellular adenomas but not the hepatocellular carcinomas should be considered as tumorigens, since they are causally related only with the benign liver lesions. Combining both benign and malignant liver tumors for statistical purposes is not justified unless each type of tumor has been affected in a statistically significant incidence. If this were not the case, classification of the agent should be in accordance with the type of lesions induced significantly. In order to use the induction of hepatocellular carcinomas in rodents as an indication of carcinogenic risk in humans appropriately, one has to verify within the limits of feasibility that the identical carcinogenic effects and the subsequent events occur both in rodents and humans.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenoma↗
PubMed2005

Development of a support vector machine-based image analysis system for assessing the thyroid nodule malignancy risk on ultrasound.

An SVM-based image analysis system was developed for assessing the malignancy risk of thyroid nodules. Ultrasound images of 120 cytology confirmed thyroid nodules (78 low-risk and 42 high-risk of malignancy) were manually segmented by a physician using a custom developed software in C++. From each nodule, 40 textural features were automatically calculated and were used with the SVM algorithm in the design of the image analysis system. Highest classification accuracy was 96.7%, misdiagnosing two high-risk and two low-risk thyroid nodules. The proposed system may be of value to physicians as a second opinion tool for avoiding unnecessary invasive procedures.

Algorithms↗
PubMed1996

Transforming growth factor-beta (TGF-beta) in silicosis.

Silicosis is characterized by fibrosing nodular lesions that may eventually develop into progressive massive fibrosis (PMF). Cytokines (interleukin-1beta [IL-1beta], tumor necrosis factor-alpha [TNF-alpha] and growth factors insulin-like growth factor-1 [IGF-1] platelet-derived growth factor [PDGF]) have been implicated in the formation of these lesions. TGF-beta promotes extracellular matrix accumulation by upregulating collagen and fibronectin gene expression, and inhibits matrix degradation by decreasing secretion of proteases and increasing secretion of protease inhibitors. We hypothesized that TGF-beta is associated with matrix deposition and fibrosis in silicosis. To test this hypothesis we studied early and late nodular lesions and PMF (11 cases and two controls) with immunohistochemistry, using rabbit polyclonal antibody to the purified whole molecule of TGF-beta in Bouin's fixed lung tissue. This antibody is reactive with both intra- and extracellular forms of TGF-beta. In the control lungs, small amounts of TGF-beta were present in the bronchial epithelium, macrophages, bronchial and vascular smooth muscle, and bronchial glands. There was minimal to moderate staining in the early silicotic peribronchiolar lesions. In the nodular lesions of silicosis, central hyalinized areas contained the maximum staining for TGF-beta. Fibroblasts in the periphery of the nodular lesions were also positive. In acute silicosis, there was marked staining of hyperplastic alveolar epithelium. Macrophages were markedly positive. In the PMF lesions, large areas of scar tissue contained TGF-beta. These data suggest a major role for TGF-beta in silicosis, particularly in the formation of silicotic nodules and the development of PMF.

Adult↗
PubMed2000

High resolution computed tomography and MRI for monitoring lung tumor growth in mice undergoing radioimmunotherapy: correlation with histology.

A model lung tumor system has been developed in mice for the evaluation of vascular targeted radioimmunotherapy. In this model, EMT-6 mammary carcinoma tumors growing in the lung are treated with 213Bi, an alpha particle emitter, which is targeted to lung blood vessels using a monoclonal antibody. Smaller tumors (< 100 microm in diameter) are cured, but larger tumors undergo a period of regression and then regrow and ultimately prove lethal. The goal of this work was to determine if external imaging with MRI or CT could be used routinely to monitor the growth/ regression of lung tumors in live mice. To attempt to evaluate individual tumors in vivo, animals were initially imaged with magnetic resonance imaging (MRI). High resolution MRI images could be obtained only after sacrifice when lungs were not moving. In contrast, high resolution computed tomography (CT) produced evaluable images from anesthetized animals. Serial CT images (up to 5/animal) were collected over a 17 day period of tumor growth and treatment. When tumored animals became moribund, animals were sacrificed and lungs were inflated with fixative, embedded in paraffin, and then sectioned serially to compare the detection of tumors by high resolution CT with detection by histology. CT proved most useful in detecting lung tumors located in the hilar area and least useful in detecting serosal surface and anterior lobe tumor foci. Overall, CT images of live animals revealed tumors in approximately 2/3 of cases detected in histologic serial sections when relatively few tumors were present per lung. Detection of lesions and their resolution post therapy were complicated due to residual hemorrhagic, regressing tumor nodules and the development of lung edema both of which appeared as high density areas in the CT scans. We conclude that the microCT method used could identify some lung tumors as small as 100 microm in diameter; however, no concrete evaluation of therapy induced regression of the tumors could be made with CT analyses alone.

Animals↗
PubMed2003

The Lotus japonicus ndx gene family is involved in nodule function and maintenance.

To elucidate the function of the ndx homeobox genes during the Rhizobium-legume symbiosis, two Lotus japonicus ndr genes were expressed in the antisense orientation under the control of the nodule-expressed promoter Psenod12 in transgenic Lotus japonicus plants. Many of the transformants obtained segregated into plants that failed to sustain proper development and maintenance of root nodules concomitant with down-regulation of the two ndx genes. The root nodules were actively fixing nitrogen 3 weeks after inoculation, but the plants exhibited a stunted growth phenotype. The nodules on such antisense plants had under-developed vasculature and lenticels when grown on medium lacking nitrogen sources. These nodules furthermore entered senescence earlier than the wild-type nodules. Normal plant growth was resumed upon external addition of nitrogen. This suggests that assimilated nitrogen is not properly supplied to the plants in which the two ndx genes are down-regulated. The results presented here, indicate that the ndx genes play a role in the development of structural nodule features, required for proper gas diffusion into the nodule and/or transport of the assimilated nitrogen to the plant.

Cell Nucleus↗
PubMed2005

Risk factors associated with development of poxvirus lesions in hospitalized California sea lions.

OBJECTIVE: To identify risk factors that may predispose California sea lions (Zalophus californianus) to development of cutaneous poxvirus nodules during hospitalization in a rehabilitation center. DESIGN: Retrospective case-control study. ANIMALS: 90 California sea lions admitted to a rehabilitation center. PROCEDURE: Hospital records of 275 stranded California sea lions admitted to the rehabilitation center between January 1 and December 31, 2002, were reviewed. All California sea lions (n = 18) that developed > or = 1 cutaneous poxvirus nodule during hospitalization were classified as cases. Seventy-two California sea lions that did not develop poxvirus lesions during hospitalization were randomly selected (control group). The frequencies of various exposure factors prior to admission, at admission, and during hospitalization for cases and control sea lions were compared by use of logistic regression. RESULTS: California sea lions that had previously been admitted to the rehabilitation center were 43 times as likely to develop poxvirus lesions as sea lions admitted for the first time; those with high band neutrophil counts (> 0.69 X 10(3) bands/microL) at admission were 20 times less likely to develop poxvirus lesions than sea lions with counts within reference limits. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that sea lions with a history of prior hospitalization or band neutrophil counts within reference limits at admission were more likely to develop poxvirus lesions during hospitalization. Sea lions with histories of hospitalization should be kept in quarantine and infection control measures implemented to help prevent disease transmission to attending personnel and other hospitalized animals.

Animals↗
PubMed1986

Lupus erythematosus panniculitis with partial genetic deficiency of C2 and C4 in a child.

A 7-year-old girl developed recurrent febrile nodules and subcutaneous plaques on her arm, shoulder, and face. Primary acquired toxoplasmosis was diagnosed at onset, because of associated lymphadenopathy and detection of specific IgM. Skin lesions were responsive to therapy with systemic steroids but progressed to atrophy and poikiloderma within a few months. Subsequently, chloroquine therapy has been instituted and no relapse has occurred. Histopathologic findings and direct immunofluorescence studies were diagnostic of lupus erythematosus panniculitis. Electron microscopy showed lamellar inclusions within mast cells. Results of laboratory investigations disclosed leukopenia and hypocomplementemia with low C2 serum levels. A family study of the complement system, including C4 and Bf phenotyping and HLA A, B, and DR haplotyping, revealed the carriage of both C2 and C4A null alleles in the propositus. This observation suggests an additional link between lupus erythematosus panniculitis and the remainder of the lupus erythematosus clinical spectrum.

Adolescent↗
PubMed1991

Treatment of human melanoma hepatic metastases in nude mice with human cytotoxic T lymphocytes.

We investigated the effects of human melanoma-specific cytotoxic T lymphocytes in treating experimental human melanoma hepatic metastases in a nude mouse model of adoptive immunotherapy. Hepatic metastases were generated by intrasplenic injection of 1.5 x 10(6) human melanoma cells. Three days after injection, animals received salt solution and interleukin 2 or interleukin 2 and cytotoxic T lymphocytes. Twenty-four of 25 control animals had developed multiple tumor nodules in the liver; 11 of 13 animals receiving only interleukin 2 also had significant tumor burdens. In striking contrast, 17 of 18 animals receiving cytotoxic T lymphocytes and interleukin 2 had no gross or histologic evidence of tumors. The remaining animal had a 2-mm nodule. Human tumor-specific cytotoxic T lymphocytes are effective in vivo in a model of adoptive immunotherapy and may prove useful in adoptive immunotherapy of humans with metastatic melanoma.

Animals↗
PubMed1978

B-cell leukemia-lymphoma with striking resemblance to Burkitt lymphoma in a 70-year-old woman.

A 70-year-old woman developed acute leukemia and a serum IgM spike. She entered complete remission with an adriamycin, vincristine, cytosine arabinoside, and prednisone combination. Bone marrow remission was maintained with intermittent cytosine arabinoside; however, she developed large skin nodules which partly remitted following adriamycin, vincristine, cyclophosphamide, and prednisone combination. They very rapidly recurred, and she died soon after. Autopsy revealed extensive tumor in the abdomen, pelvis, and thoracic cavity, but no bone marrow involvement. Histology revealed a "starry sky" appearance. Cytology showed undifferentiated cells with vacuolated cytoplasm resembling Burkitt lymphoma cells. Peroxidase and esterase stains were negative. There was strong pyroninophilia and the periodic acid-Schiff reaction showed granular activity in the cytoplasm. Electron microscopic appearances also resembled Burkitt lymphoma. Cytogenetic studies were normal, with no Ph1 chromosome. Immunofluorescence demonstrated surface IgM and a little IgA. 3H-thymidine incorporation was high, indicating rapid growth. Dibutyral cyclic adenosine monophosphate (cAMP) stimulated growth, which was further evidence of the lymphoid origin of the tumor. The close resemblance of this tumor to Burkitt lymphoma emphasizes the difficulties in systematically classifying the lymphomas.

Acute Disease↗
PubMedDate not supplied

Rheumatoid nodulosis: an unusual variant of rheumatoid disease.

A middle-aged man developed multiple subcutaneous nodules associated with palindromic rheumatism. There was little evidence of synovitis; however multiple cyst-like intraosseous radiolucencies were noted. Nodules from two sites were histologically typical rheumatoid nodules. Subjective and objective improvement occurred during penicillamine therapy. This clincial presentation seems sufficiently distinctive to warrant characterization as a variant of rheumatoid disease termed by us: rheumatoid nodulosis.

Arthritis↗