Biomedical subjects
Publications and source records attributed to M S Fisher.
This is a case of aspergillosis of the bone and soft tissues of the chest wall in a (probably) immunocompetent host. The areas of involvement and different types of this disease are described. The A. flavus group, which presumably was responsible for this involvement of the chest wall, is very uncommon as a pathogen in humans.
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Ultraviolet (UV)-irradiated mice were compared with unirradiated mice for their susceptibility to primary and transplanted tumors etiologically unrelated to UV radiation. Although UV-irradiated mice are unable to reject transplants of highly antigenic syngeneic tumors induced by UV light, the growth of syngeneic, non-UV-induced tumors generally was not accelerated in these animals. Furthermore, UV-irradiated mice were no more susceptible to the induction of primary leukemias, mammary tumors, or sarcomas than were unirradiated animals. Tests of immune responses to weak transplantation antigens showed that UV-irradiated mice rejected H-Y-incompatible skin grafts as vigorously as did normal animals, and that the primary in vitro cytotoxic responses of spleen cells from UV-irradiated mice to trinitrophenyl (TNP)-modified syngeneic cells and to Hh antigens were unaffected. We conclude that the susceptibility of UV-irradiated mice to challenge with UV-induced tumors represents a selective unresponsiveness, and that it is not attributable to a generalized deficiency in the immune response to tumor-specific antigens or to weak transplantation antigens.
Recent studies have suggested that the immunologic unresponsiveness of UV-irradiated mice against UV-induced fibrosarcomas might be due to the presence of suppressor lymphoid cells. In these experiments, we present additional evidence that suppressor lymphoid cells are present in lymph nodes and spleens of UV-irradiated mice and demonstrate that these cells are enriched after incubation on nylon wool columns, that they are inactive after treatment with anti-theta serum and complement, and that they are effective for at least 7 weeks after transfer to lethally x-irradiated mice. Splenectomy of UV-treated mice before tumor challenge did not restore their anti-tumor reactivity. The UV-induced suppressor cells appear to be specific for syngeneic UV-induced tumors, since they did not suppress the rejection of an allogeneic UV-induced tumor or two chemically induced syngeneic tumors.
Chronic treatment of mice with UVR not only induced skin cancer but also produced a systemic change that interfered with host resistance against these tumors. The studies leading to the this conclusion were prompted by the discovery that most tumors induced in C3H mice by chronic UV irradiation were immunologically rejected following transplatation to normal syngeneic recipients. This raised the question of why these tumors were able to grow progressively in the autochthonous host without being destroyed immunologically. We found that after a short course of UV treatment, the UV-irradiated mice lost their ability to reject transplanted UV-irradiated mice lost their ability to reject transplanted UV-induced tumors, even though such transplants were rejected by unirradiated animals. The growth of the transplanted tumors in UV-treated mice resulted from a systemic alteration in the animals that was induced by UV irradiation of the skin.
Chronic irradiation of mice with UV light produces a systemic alteration that is immunologic in nature and may be due to the presence of specific suppressor lymphoid cells. The immunologic aspect of this systemic alteration was demonstrated by cell transfer experiments. Lymphoid cells from UV-treated donors were unable to confer tumor resistance to lethally X-irradiated and neonatal liver reconstituted recipients, whereas recipients given lymphoid cells from normal donors were resistant to a challenge with a syngeneic UV-induced tumor. Therefore, lymphoid cells from normal donors could mediate tumor rejection, but lymphoid cell from UV-irradiated donors could not. Furthermore, lymphoid cells from UV-treated donors suppressed the ability of lymphoid cells from normal donors to mediate syngeneic tumor rejection when mixed 1:1 before transfer into lethally X-irradiated recipients. This suppression was specific since all recipients recipients resisted an allogeneic UV-induced tumor challenge. Serum transfer experiments failed to demonstrate any inactivating or suppressive substances in the serum of UV-treated animals. The findings suggested that UV-treated mice failed to reject UV-induced tumors because UV irradiation induced specific suppressor lymphoid cells that prevented the development of an immune respons against these tumor antigens.
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Chronic irradiation of mice with ultraviolet (UV) light produces a systemic alteration of an immunologic nature. This alteration is detectable in mice long before primary skin cancers induced by UV light begin to appear. The alteration results in the failure of UV-irradiated mice to reject highly antigenic, transplanted UV-induced tumors that are rejected by unirradiated syngeneic recipients. The immunologic aspect of this systemic alteration was demonstrated by transferring lymphoid cells from UV-irradiated mice to lethally x-irradiated recipients. These recipeints were unable to resist a later challenge with a syngeneic UV-induced tumor, whereas those given lymphoid cells from normal donors were resistant to tumor growth. Parabiosis of normal mice with UV-irradiated mice, followed by tumor challenge of both parabionts with a UV-induced tumor, resulted in the growth of the challenge tumors in both UV-irradiated and unirradiated mice. Splenic lymphocytes from tumor-implanted UV-treated mice were not cytotoxic in vitro against UV-induced tumors, whereas under identical conditions cells from tumor-implanted, unirradiated mice were highly cytotoxic. Our findings suggest that repeated UV irradiation can circumvent an immunologic mechanism that might otherwise destroy nascent UV-induced primary tumors that are strongly antigenic.
In these experiments, we tested in various in vivo assays the immune responses of inbred C3H/HeN(MTV-) (C3H-) mice during carcinogenesis by chronic exposure to UV irradiation. Although the UV-treated mice were unable to reject syngeneic UV-induced tumor transplants, they rejected H-2-incompatible tumor allografts and H-2-compatible skin allografts. The primary hemagglutinin response to sheep red blood cells was normal in these mice, as were the induction of a local graft-versus-host reaction with lymphoid cells from UV-irradiated donors and the induction of an inflammatory response to dimethyl sulfoxide in the footpads of UV-treated mice. An early transient depression of two reactions in UV-irradiated mice occurred: delayed hypersensitivity to dinitrochlorobenzene measured by footpad swelling and the graft-versus-host reaction in UV-irradiated recipients measured by the use of the popliteal lymph node weight gain assay. Both of these reactions returned to a normal level before the development of primary tumors. We conclude that the inability of UV-irradiated mice to reject syngeneic and autochthonous UV-induced tumors was not due to a generalized immunosuppressive effect of chronic UV irradiation.
Tumor metastatic to the esophagus is a rare lesion. Two cases, primary in pancreas and rectum, are described. There are no distinguishing radiologic features.
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Skin tumors induced in mice by UV light are usually immunologically rejected by normal syngeneic recipents. We evaluated the immune status of primary hosts against these highly antigenic tumors immediately after surgical removal of the primary tumor. All primary hosts were susceptible to challenge with their autochthonous tumors, though most of these were rejected by untreated control mice. Primary hosts were also susceptible to challenge with isografts of antigenically dissimilar UV-induced neoplasms. The susceptibility of the primary hosts to tumor challenge was probably induced by chronic exposure to UV light, since UV-irradiated non-tumor-bearing mice were also susceptible to challenge with these tumors. Although UV-treated mice were unalbe to reject these syngeneic tumors, they could reject skin and tumor allografts. Further, UV irradiation did not interfere with the second-set rejection of syngeneic UV-induced tumors in mice that were specifically immunized before UV treatment.
A patient with a mobile mass of anaerobic organisms in the pulmonary parenchyma is presented. Radiographically it resembled a fungous ball. This observed botryomycoma may be part of the spectrum of aspiration pneumonia.
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Areas of sclerosis in the phalanges, particularly the terminal phalanges, are common in sarcoidosis despite the rarity of osteosclerotic changes in other bones. Of 37 patients with sarcoidosis with osseous changes of the hands or feet, 20 (54%) has sclerosis either alone or in combination with bone destruction. Of 48 patients with acrosclerosis, 20 (40%) had sarcoidosis. In the authors' experience with a largely black population, sarcoidosis was found to be the most common causes of acrosclerosis.
Uterine artery calcification was observed in 26 patients. Fourteen of the 22 with adequate cliniccal information had diabetes mellitus. This is considered a significant association by the authors and calcification should raise the question of diabetes.
Although pigment melanin has long been though of as "inert," recent work has attested to its chemical reactivity. In this communication, we report that either commercial synthetic melanin prepared by persulfate oxidation of tyrosine ("Sigma melanin") or sepia melanin extracted from cuttlefish markedly accelerates the in vitro oxygenation of p-hydroxyanisole (MMEH), catalyzed by mushroom or B-16 melanoma tyrosinase. Kinetics of 4-methoxy-1,2-benzoquinone formation (lambda max = 413 nm) or of molecular O2 uptake were biphasic, with an initial slow rate ("lag time") followed by a fast linear increase. The biphasic response reflects an initial slow hydroxylation followed by a fast dehydrogenation. Added melanin markedly decreased the lag time but had little effect on subsequent dehydrogenation. Similar effects were observed for tyrosine itself. A complex between MMEH and melanin appears to be the "active" species in these reactions. The results indicate that melanin acts as an electron conduit, which accepts electrons from the substrate and transfers them to tyrosinase. The magnitude of the effect depends on the type of melanin as well as on its oxidation state. Kinetic analysis indicates that both melanins are very efficient at transferring electron to tyrosinase, and that Sigma melanin is roughly threefold more efficient than sepia melanin. The qualitative similarity of reaction between the synthetic and "natural" melanins suggests that the former may serve as a first approximation to the in vivo situation. On the other hand, the observed quantitative differences and the sensitivity of these results to the chemical state of melanin suggests that this methodology might eventually be adapted as a non-destructive probe of melanin in situ.(ABSTRACT TRUNCATED AT 250 WORDS)