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Biomedical subjects

V Tron

Publications and source records attributed to V Tron.

At least 19 recordsLinked to original sources
PubMed1998

Induction of squamous cell carcinoma in p53-deficient mice after ultraviolet irradiation.

Mutations of the p53 gene have been implicated as an important factor in the pathogenesis of ultraviolet light induced skin cancers. To examine the role of p53 in skin carcinogenesis, we observed the development of skin cancers in homozygous p53-deficient (-/-) mice and wild-type p53 (+/+) mice, after chronic ultraviolet B (290-320 nm) exposure. At a dose of 2 J per m2 per s of ultraviolet B for 30 min three times per week, all p53-/- mice developed skin tumors by week 12. All the p53-/- mice developed multiple tumors by week 16. The majority of the tumors occurred on the ears. None of the p53+/+ mice developed skin tumors after 17 wk of UV exposure. Ten p53-/- tumors were examined histologically: five invasive squamous cell carcinomas, four squamous cell carcinomas in situ, and one actinic keratosis. p53-/- mice have a short life-span due to internal tumors or a deficiency in the immune system; however, ultraviolet B exposure did not significantly reduce the life-span of p53-/- mice. These results demonstrate that loss of wild-type p53 function shortens the latent period and predisposes the animals to the development of squamous cell carcinomas after ultraviolet irradiation.

Alleles↗
PubMed1998

Chemotherapy-induced apoptosis in melanoma cells is p53 dependent.

Metastatic melanomas are often resistant to chemotherapy. To study whether the p53 mutational status affects chemosensitivity, we compared the responses to chemotherapy of four melanoma cell lines containing the wild-type p53 and four cell lines carrying the mutant p53. Cisplatin, at 10 microM, virtually killed all the cells in the wild-type p53 cell lines, while 57-95% of the cells in the mutant p53 cell lines survived (P = 0.005). After treatment with 100 nM of vincristine, on average 18% of the wild-type p53 melanoma cells survived compared with 55% of the mutant p53 cells (P = 0.04). After treatment with 40 nM, 200 nM or 1 microM of camptothecin the survival rates were, on average, 16%, 8% and 4% for the wild-type p53 melanoma cells, compared with 89%, 67% and 38% for the mutant p53 cells, respectively (P = 0.00004, P = 0.003 and P = 0.04, respectively). The anticancer agents were not toxic to normal melanocytes at doses inducing cytotoxicity in wild-type p53 melanoma cells. The main mechanism of cytotoxicity appears to be drug-induced apoptosis. Cisplatin, camptothecin and vincristine all induced apoptosis in wild-type p53 melanoma cells, but not in mutant p53 cells. Our results suggest that chemotherapy-induced apoptosis in melanoma cells is p53 dependent, and mutation of the p53 gene is an indicator of drug resistance in melanoma.

Antineoplastic Agents↗
PubMed1995

Wells' syndrome in childhood: case report and review of the literature.

We report a severe case of Wells' syndrome, or eosinophilic cellulitis, after a bee sting in a 4-year-old girl. The patient had a widespread, painful, blistering eruption that was subsequently complicated by Pseudomonas aeruginosa superinfection and septicemia, hypoalbuminemia, anemia, and neutropenia. The skin lesions responded to systemic steroid therapy. There was residual scarring alopecia of the scalp. There have been 17 previous reports of childhood Wells' syndrome. We believe that this disorder is a distinct entity that should be considered in the differential diagnosis of blistering diseases in children.

Animals↗
PubMed1995

CD-34 expression.

Explore the source record for details and available documents.

Antigens, CD↗
PubMed1993

Treatment of chronic severe alopecia areata with topical diphenylcyclopropenone and 5% minoxidil: a clinical and immunopathologic evaluation.

BACKGROUND: Topical diphenylcyclopropenone (DPCP) and minoxidil have been used in the treatment of alopecia areata with variable results. OBJECTIVE: This study was designed to evaluate the efficacy of DPCP alone or in combination with topical 5% minoxidil for the treatment of chronic severe alopecia areata. The effect of therapy on cutaneous T-cell and Langerhans cell subpopulations and intercellular adhesion molecule-1 (ICAM-1) expression was also examined. METHODS: Fifteen patients with chronic (more than 2 years), severe (more than 50% scalp involvement) alopecia areata participated in a 24-week trial. Half of the scalp was treated with DPCP once weekly and with either 5% minoxidil solution or a vehicle solution twice daily in a randomized double-blind design. Skin biopsy specimens from each half of the scalp were obtained before therapy and after 12 and 24 weeks of therapy for histologic and immunophenotypic analysis. RESULTS: Thirteen patients completed the study. Five of 13 patients (38%) showed marked regrowth of coarse terminal hair after 24 weeks of treatment with DPCP. The addition of topical 5% minoxidil did not produce any significant clinical benefit in this 24-week trial. Immunophenotypic analysis showed no differences between responders and nonresponders at baseline. During treatment, Leu-4, Leu-2, Leu-3, and keratinocyte ICAM-1 expression were significantly reduced in biopsy specimens of responders versus nonresponders. CONCLUSION: DPCP treatment showed a 38% success rate in producing cosmetically acceptable regrowth in patients with chronic severe alopecia areata.

Administration, Cutaneous↗
PubMed1991

Evaluation of cartilage lesions by magnetic resonance imaging at 0.15 T: comparison with anatomy and concordance with arthroscopy.

Recent evidence suggests that pharmacological treatment may alter the rate of progression of cartilage damage in osteoarthritis (OA). However, a lack of accurate and precise noninvasive assessments of cartilage structure makes it difficult to answer this question directly with prospective clinical trials, prevents early diagnosis of OA and restricts assessment of treatment to evaluation of symptoms or joint function. It is important, therefore, to develop precise, noninvasive methods both for diagnosis of early OA before damage is extensive and irreversible and for evaluation of therapeutic effectiveness. Magnetic resonance imaging (MRI) allows for noninvasive, multiplanar body imaging which depends on proton density, flow, and the T1 and T2 relaxation times. Because these variables differ markedly among joint tissues, cartilage erosions are visible with MRI and it should be possible to quantify them. Our objective was to compare MRI with arthroscopy for assessing the depth of lesions in the articular cartilage of human knees to help develop and validate MRI for use in clinical trials designed to assess the effect of therapy on cartilage structure. In the first part of our study, the effect of the MRI pulse sequence variables on the images was evaluated by varying them systematically and comparing the anatomy seen with MRI with that seen at arthroscopy or arthrotomy and with the histology. In the second part, 31 patients were assessed with MRI before arthroscopy. The MRI were graded on a 4-point ordinal scale by 2 observers who were unaware of the clinical diagnosis and compared with findings at arthroscopy which were graded using the same scale.(ABSTRACT TRUNCATED AT 250 WORDS)

Arthroscopy↗
PubMed1988

Cigarette smoke potentiates asbestos-induced airflow abnormalities.

It has been suggested that exposure to both asbestos and cigarette smoke can produce worse parenchymal lung disease than exposure to asbestos alone. Using a guinea pig model of asbestos administration that produces primarily airway disease and associated airflow abnormalities, we showed previously that the combination of asbestos and smoke acts synergistically to produce more marked increases in tissue collagen, fibrosis of airway walls, and early interstitial fibrosis than are seen with asbestos alone. To investigate the functional effects of these morphological and biochemical abnormalities, pulmonary function tests for volumes and flows, including lung volumes, pressure-volume curves, and flow-volume curves, were performed. By themselves, both smoke and asbestos produced increases in total lung capacity (TLC), residual volume (RV), and functional residual capacity (FRC); the two agents together made all these changes worse than either one alone. Both smoking and asbestos moved the pressure-volume curve upward, and the effects of the two agents together were again greater than either alone. Similarly, both smoke and asbestos decreased flows, and the two agents produced more severe impairment than either one by itself. The changes in volumes, pressure-volume curve, and flows correlated with both increased thickness of small airway walls and increases in airspace size. These observations indicate that, at least in this guinea pig model, cigarette smoke can potentiate the functional consequences of asbestos exposure.

Asbestos↗
PubMed1987

Cigarette smoke makes airway and early parenchymal asbestos-induced lung disease worse in the guinea pig.

In order to assess the effects of cigarette smoke and asbestos exposure, we divided guinea pigs into 4 groups: smoking or nonsmoking, and asbestos-exposed or not asbestos-exposed groups. Asbestos-exposed animals were given a single intratracheal instillation of 5 mg UICC amosite, a dose and method of administration that we have previously shown produces morphologic changes in the small airways as well as minimal interstitial fibrosis. Animals were smoked 5 days per week for 6 months. By itself, smoking did not affect lung collagen content, small airways wall thickness, or the volume fraction of tissue surrounding airways, but it did cause a significant increase in alveolar mean linear intercept (Lm). Asbestos alone increased collagen content, airway wall thickness, and tissue volume fraction surrounding airways, the latter measure used to assess interstitial fibrosis. An unexpected finding was that asbestos also increased Lm. The two agents administered together caused more severe changes of all types than were produced by either agent alone, and the interaction between the 2 was generally synergistic. Smoke-exposed animals retained 3 times the asbestos fiber burden of those not smoke-exposed; the increase in retention was greater for short than for long fibers. We conclude that cigarette smoke can potentiate the fibrosis induced by asbestos, possibly because of increased fiber retention. As well, in this model, asbestos or asbestos plus cigarette smoke produces increases in alveolar size.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Allergic angiitis of Churg and Strauss syndrome. Response to pulse methylprednisolone.

Our patient presented with widespread airspace consolidation. He was a steroid-dependent asthmatic receiving moderate doses of corticosteroid therapy. Open lung biopsy showed allergic angiitis of Churg and Strauss syndrome. The patient continued to deteriorate on high doses of prednisone. He was subsequently given four pulses of intravenous methylprednisolone with dramatic clearing noted on x-ray film and resolution of his shunt.

Adult↗
PubMed1987

Carcinoembryonic antigen and milk-fat globule protein staining of malignant mesothelioma and adenocarcinoma of the lung.

Immunohistologic markers have been of considerable value in differentiating malignant mesothelioma from adenocarcinoma. Recently, staining for milk-fat globule (MFG) protein has been suggested as a useful diagnostic test for this separation, but subsequent reports have been conflicting, with some authors finding clearcut differences, while others showed similar marking of both tumor types. To examine this technique further, we studied lung carcinomas and mesotheliomas with commercially available anti-MFG, and compared these results with those obtained with anticarcinoembryonic antigen (CEA), a commonly used immunomarker of carcinoma. We found that carcinomas showed strong cytoplasmic staining for MFG and CEA; however, a greater percentage of carcinomas were more strongly positive for CEA than for MFG. Mesotheliomas did not, for the most part, stain strongly with either antibody. In addition, carcinomas from different hospitals stained differently for MFG, but not for CEA. We conclude that although strong cytoplasmic staining for MFG is a reasonably reliable indicator of carcinoma, CEA staining provides a better separation and is considerably easier to interpret in lung cancer specimens.

Adenocarcinoma↗
PubMed1987

Effects of cigarette smoke exposure on retention of asbestos fibers in various morphologic compartments of the guinea pig lung.

For investigation of mechanisms whereby smoking might potentiate asbestos-related disease, guinea pigs were given 0.5 mg UICC amosite by intratracheal instillation. Half the animals were subsequently exposed to cigarette smoke. Animals were sacrificed at 1 day, 7 days, and 1 month after exposure. Lungs were lavaged and macrophages separated from the lavage fluid. Lung fiber concentration, numbers of fibers in macrophages, and fiber sizes from tissue (TFs), macrophages (MFs), and macrophage-free lavagate (FFs) were determined by electron microscopy. Smoke-exposed animals retained greater numbers of fibers in lung tissue by 1 month but had greater total numbers of fibers in macrophages at all time periods. In both smokers and nonsmokers, fibers in the three morphologic compartments had distinctly different lengths: the longest fibers were found associated with the lung tissue; the macrophages always contained the shortest fibers; and the macrophage-free lavagate had fibers of intermediate size. However, fiber widths and aspect ratios did not show the same clear separation by anatomic compartment, suggesting that in both smoking and nonsmoking animals length is the size parameter which is most important in determining fiber clearance. Smoking did not affect the lengths of MFs but did produce a progressive reduction in the lengths of FFs and TFs with time. These data indicate that smoking causes a marked increase in the number of fibers retained in the lung within macrophages and suggest that either macrophage removal via the mucociliary escalator or macrophage mobility is impaired by cigarette smoke. However, smoking does not change the sizes of fibers in macrophages and does not appear to depress phagocytic capacity. These observations imply that failure of macrophage clearance and subsequent re-release of fibers into the medium may at least partially explain the changes in fiber sizes and eventual increases in tissue fiber concentrations in smoke-exposed animals.

Animals↗
PubMed1986

Pulmonary capillary hemangiomatosis.

Pulmonary capillary hemangiomatosis (PCH) is a rare cause of pulmonary hypertension; only three cases have been reported. Four additional cases are described in this report. All of the patients in this study presented with signs and symptoms of pulmonary hypertension, and in none was a correct morphologic diagnosis made during life. Histologically, the most striking feature was the presence of numerous cytologically benign thin-walled capillary-sized blood vessels proliferating diffusely through alveolar walls and in and around larger vessels and airways. Venous infiltration was associated with intimal fibrosis and secondary veno-occlusive disease (VOD). Because of the presence of hemorrhage, the apparent interstitial widening and inflammation, and the venous changes, the condition in these cases was initially misdiagnosed as interstitial fibrosis or VOD. However, the identification of proliferating and invasive capillaries, which are unique to PCH, led to the correct diagnosis. Although the nature of PCH is unknown, it behaves like a low-grade vascular neoplasm.

Adolescent↗
PubMed1986

Chronic necrotizing pulmonary aspergillosis mimicking bronchocentric granulomatosis.

We present a case of slowly progressive Aspergillus infection occurring in a partially immunocompromised host. The histologic pattern mimicked bronchocentric granulomatosis as seen in allergic bronchopulmonary aspergillosis, but the clinical history, spread of disease in the face of steroid therapy, peculiar granulomatous response to the organisms, and large numbers of organisms present suggest that this was really a case of chronic necrotizing pulmonary aspergillosis. These entities must be distinguished because their therapy, prognosis, and clinical significance are totally different.

Aspergillosis↗