Biomedical subjects
Publications and source records attributed to M Kyriakos.
We describe an adolescent girl with symptoms secondary to bilateral, symmetrical ganglion cysts of the scaphoid bones. From the roentgenographic and operative findings, it was believed that the cysts were the penetrating type. The patient is among the youngest reported with carpal bone ganglion cysts and the first with bilateral scaphoid cysts completely described in the English-language medical literature.
A case of intracortical osteosarcoma, a rare form of osteosarcoma that may radiologically simulate a variety of benign and malignant bone lesions, is described. To date, all cases have arisen in the diaphysis of either the tibia or femur, and histologically have been of osteoblastic type. In contrast, the current tumor was a small cell osteosarcoma, another uncommon variety of osteosarcoma. A summary of the reported cases of intracortical osteosarcoma is given, and the literature on small cell osteosarcoma is briefly reviewed.
An 11-year-old girl had a lytic, benign-appearing, expansive lesion of the distal tibia radiologically interpreted as an aneurysmal bone cyst (ABC). Tissue from two extensive curettage procedures was also histologically diagnosed as ABC. Approximately 50 months after the onset of symptoms, and 28 months after her last curettage, a highly pleomorphic osteosarcoma developed. The patient had not received prior radiation therapy. The cases in the literature of possible malignant transformation of ABC are reviewed. The authors separate their case from telangiectatic osteosarcoma, and from "aneurysmal bone cyst-like osteosarcoma."
Spleen cells from CBA/J mice immunized with mouse thyroglobulin (MTg) and the adjuvant lipopolysaccharide induce experimental autoimmune thyroiditis (EAT) after transfer to recipient mice if they are first activated in vitro with MTg. EAT induced by cells cultured with MTg is generally moderate in severity and is characterized by a thyroid infiltration consisting primarily of mononuclear cells. Addition of the anti-interleukin 2 receptor (IL-2R) monoclonal antibodies (mAbs) M7/20, 3C7, or 7D4 to spleen cell cultures with MTg resulted in a cell population capable of inducing a more severe type of EAT characterized by extensive follicular destruction, granuloma formation, and the presence of multinucleated giant cells. Recipients of cells cultured with MTg and anti-IL-2R mAb also had higher anti-MTg autoantibody responses than recipients of cells cultured with MTg alone. Activation of cells capable of transferring severe granulomatous EAT and increased anti-MTg autoantibody responses required both MTg and M7/20 in culture and required addition of M7/20 within the first 8 h of the 72-h culture period. CD4+ T cells were required for the expression of both the severe granulomatous EAT lesions and the mononuclear cell infiltrates typically observed in murine EAT. The increased anti-MTg autoantibody responses in recipients of cells cultured with MTg and anti-IL-2R mAbs were not restricted to a particular immunoglobulin G (IgG) subclass and included antibody of the IgG1, IgG2A, and IgG2B subclasses. These results suggest that a subset of CD4+ T cells capable of inducing severe granulomatous EAT and increased anti-MTg autoantibody responses is preferentially activated when cells are cultured in the presence of anti-IL-2R mAb. Anti-IL-2R mAb may either prevent activation of cells that induce classical lymphocytic EAT or prevent activation of cells that normally function to downregulate EAT effector T cell activity.
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Although "rudimentary meningocele" (RM) or "meningothelial hamartoma" of the skin is a seemingly recently described entity, it has been included in past reports as a variant of primary cutaneous meningioma. We document our experience with four such lesions and compare the histologic and immunohistochemical features of these cases with those of seven classic meningoceles (CM) and four giant cell fibroblastomas (GCF). Although all of these entities share significant points of microscopic similarity, RM and CM are lesions composed of meningothelial cells, whereas GCF is probably of myofibroblastic origin. Rudimentary and classic meningoceles demonstrate cellular immunoreactivity for vimentin and epithelial membrane antigen, whereas the cells of GCF lack the latter determinant and may express muscle-specific actin. Our observations suggest that RM and CM represent closely related developmental malformations; however, RM becomes clinically apparent in a somewhat older patient population than CM and is not associated with major skeletal anomalies as may be found with CM. The distinction between various cutaneous meningothelial proliferations has prognostic importance, as does their separation from GCF. RM and CM are adequately treated by simple excision, whereas GCF, a probable form of fibromatosis, has the potential for local recurrence.
Thirty-eight cases of histologically confirmed chondromyxoid fibroma were reviewed and their radiographic features recorded. These findings, coupled with a review of the English-language medical literature, suggest that this rare, benign bone tumor has a characteristic but not specific radiographic appearance and may often mimic more common tumors. Chondromyxoid fibroma may occur anywhere in the skeleton, but almost half of the cases occur around the knee. The possibility of chondromyxoid fibroma should always be considered when a focal bone lesion is evaluated that has geographic bone destruction, a sclerotic rim, lobulated margins, and septation. The diagnosis of chondromyxoid fibroma is most likely when the patient is in the 2nd decade of life.
Susceptibility to experimental autoimmune thyroiditis (EAT) in mice is linked to the I-A subregion of the major histocompatibility complex (MHC). The present study was undertaken to assess the effectiveness of anti-I-Ak monoclonal antibody (MAb) 10-2.16 in preventing or arresting the development of EAT. Spleen cells from CBA/J or (CBA/J x Balb/c) F1 mice given 10-2.16 prior to sensitization with mouse thyroglobulin (MTg) and adjuvant could not transfer EAT to normal recipients, and cells from these mice did not proliferate in vitro to MTg. Donor CBA/J mice given 10-2.16 before immunization and recipients of cells from such mice produced little MTg-specific IgG1 or IgG2b antibody but did produce nearly as much IgG2a as controls. The effects of in vivo treatment with 10-2.16 appear to be due to elimination of Ia + cells rather than to modulation of Ia or induction of suppressor T cells. When 10-2.16 was added to in vitro cultures it also prevented the proliferation and activation of sensitized CBA/J or F1 effector cell precursors. Other mAb specific for MHC class II gene products, but not associated with disease susceptibility, expressed by CBA/J (I-Ek) or F1 (I-Ad) mice (14-4-4S or MK-D6 respectively), also prevented in vivo sensitization, but did not block in vitro activation. Anti-I-Ak was also effective in preventing EAT if multiple injections of mAb were given to recipients of sensitized EAT effector cells.(ABSTRACT TRUNCATED AT 250 WORDS)
An asymptomatic 73-year-old woman was found to have multiple, simultaneous, inverted papillomas of the renal pelvis and ureter. A review of the world literature yielded 34 cases of inverted papillomas in the upper urinary tract: 13 in the renal pelvis, and 21 in the ureter. Among these 34 cases, there were 26 male and five female patients, with gender not given for three others. Patients ranged in age from 19 to 89 years (mean, 64.1 years). Many cases lacked complete clinical details but, among the others, gross painless hematuria was the presenting symptom in seven; hematuria with flank pain or colic in six; and pain without hematuria in six. Only six patients lacked urinary tract symptoms, and three of these had microscopic hematuria. Only two patients had more than one inverted papilloma, and these were not multicentric. Adequate pathologic documentation and follow-up data were, unfortunately, absent in many of the cases. Although inverted papillomas are curable with surgical resection, with a low rate of local recurrence, they appear to be associated with synchronous or asynchronous carcinomas, especially other transitional cell tumors in the urinary tract.
Malignant fibrous histiocytoma (MFH) is among the most common soft tissue sarcomas of adult life, but rarely occurs elsewhere. We report an example of primary MFH of the lung and review 15 previously reported acceptable cases with current follow-up information. Histologically, the tumor in our case was pleomorphic with storiform and fascicular areas. Tumor cells showed positive immunostaining for alpha 1-antitrypsin, alpha 1-antichymotrypsin, and vimentin. Stains for desmin, cytokeratin, myoglobin, epithelial membrane antigen, S-100 protein, and lysozyme were negative. Electron microscopic study showed histiocyte-like, fibroblast-like, intermediate, and undifferentiated tumor cells. A variety of methods were used to treat these patients. Two patients survived for 5 or more years, two were alive and well at 8 and 12 months, respectively, two were alive with metastatic tumor at 3 and 18 months, respectively, and ten patients died of tumor, with an average survival of 1 year.
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Experimental autoimmune thyroiditis (EAT) can be induced in CBA/J mice following the transfer of spleen cells from mouse thyroglobulin (MTg)-sensitized donors that have been activated in vitro with MTg. Since L3T4+ T cells are required to transfer EAT in this model, the present study was undertaken to assess the effectiveness of the anti-L3T4 monoclonal antibody (mAb) GK1.5 in preventing or arresting the development of EAT. Spleen cells from mice given mAb GK1.5 prior to sensitization with MTg and adjuvant could not transfer EAT to normal recipients and cells from these mice did not proliferate in vitro to MTg. Donor mice given GK1.5 before immunization did not develop anti-MTg autoantibody and recipients of cells from such mice also produced little anti-MTg. GK1.5 could also prevent the proliferation and activation of sensitized effector cell precursors when added to in vitro cultures. When a single injection of mAb GK1.5 was given to recipients of in vitro-activated spleen cells, EAT was reduced whether the mAb was given prior to cell transfer or as late as 19 days after cell transfer. Whereas the incidence and severity of EAT was consistently reduced by injecting recipient mice with GK1.5, the same mice generally had no reduction in anti-MTg autoantibody. Since EAT is consistently induced in control recipients by 14-19 days after cell transfer, the ability of mAb GK1.5 to inhibit EAT when injected 14 or 19 days after cell transfer indicates that a single injection of the mAb GK1.5 can cause reversal of the histopathologic lesions of EAT in mice. These studies further establish the important role of L3T4+ T cells in the pathogenesis of EAT in mice and also suggest that therapy with an appropriate mAb may be an effective treatment for certain autoimmune diseases even when the therapy is initiated late in the course of the disease.
In a review of 364 radiocarpal and 123 distal radioulnar joint arthrograms we identified 44 (12%) patients with contrast defects at either the proximal or distal surface of the carpal triangular fibrocartilage complex (TFCC). Differences in their arthrographic characteristics distinguished two separate groups of patients; one with similar and another with dissimilar appearing TFCC surface contrast collections. Thirty-one of our 44 patients had similar appearing, isolated radial-sided collections at either the proximal or distal TFCC surfaces. Our arthrographic, demographic, and historical study of these patients suggests that the collections are not caused by traumatic partial TFCC tears but represent a normal anatomic variant, probably a synovial recess at the radial TFCC attachment. Arthrography and dissection of a limited number of cadaveric specimens confirmed this conclusion. The second group included the remaining 13 patients. This group had contrast collections at either the proximal or distal TFCC surface, which varied in location and appearance. This smaller group is more likely to represent those uncommon patients with partial TFCC defects caused by tears.
An example of malignant fibrous histiocytoma (MFH) of the stomach, manifesting initially as a pulmonary metastasis, is described. A review of the world medical literature yielded ten other examples of MFH of the alimentary tract--four in the large intestine, two each in the small intestine and rectum, and one each in the esophagus and stomach. Patients ranged in age from 17 to 74 years, and all but one were males. Histologically, 91% of the tumors were of the pleomorphic type, with or without an associated storiform pattern. Six of the 11 patients died, two postoperatively and four with tumor, while the others were alive from 14 months to eight years after therapy. The distinction between gastric MFH and leiomyosarcoma is discussed.
Experimental autoimmune thyroiditis (EAT) can be adoptively transferred to normal syngeneic recipients using spleen cells from susceptible strains of mice primed in vivo with mouse thyroglobulin (MTg) and lipopolysaccharide (LPS) following in vitro activation of spleen cells by culture with MTg. Irradiation of recipient animals markedly augments the severity of thyroiditis induced in this system. Irradiation of recipients does not alter the time course of the development of thyroiditis, nor does it alter the requirement for both in vivo priming and in vitro activation of spleen cells for the development of EAT. Spleen cells from EAT-resistant strains of mice (e.g., Balb/c) do not induce EAT in irradiated recipients. Irradiated recipients develop significant levels of anti-MTg antibodies while unirradiated recipients have little detectable antibody response. The augmenting effect of irradiation can be substantially reversed by transferring naive spleen cells to recipients prior to the transfer of MTg/LPS-primed in vitro-activated spleen cells. In addition athymic CBA/Tufts nude mice develop more severe EAT than CBA/Tufts nude/+ littermates following transfer of activated CBA/J spleen cells. These data suggest that natural suppressor cells may regulate the development of EAT at the effector cell level.
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Explore the source record for details and available documents.